Science Today

Small Protein, Big Impact: Microprotein Discovery Offers Hope for Obesity and Aging

noreply@blogger.com (Unknown) — Tue, 02 Sep 2025 01:45:00 +0000

Researchers have uncovered a tiny but powerful protein that helps keep our cells’ energy factories humming – a discovery that could spark new approaches to tackling obesity and age-related decline. Scientists at the Salk Institute in La Jolla found that a “microprotein” in mouse fat cells plays a critical role in maintaining healthy mitochondria, the structures that generate energy in our cells. By preserving mitochondrial function, this diminutive protein helps cells burn fuel efficiently, which in turn could influence body weight and the aging process. The findings shine light on how molecular biology connects to everyday health, opening the door to science-backed strategies for better metabolismand longevity.

Mature brown fat cells from a mouse, with the newly discovered microprotein shown in red inside mitochondria (green) and nuclei in blue. This tiny protein helps preserve mitochondrial health under stress. (Credit: Salk Institute)

Mighty Mitochondria in Every Cell: Often dubbed the “powerhouses of the cell,” mitochondria convert the food we eat into usable energy. They are especially active in brown fat – a type of body fat that burns calories to produce heat and regulate body temperature. (Most fat tissue is white fat, which primarily stores energy.) When activated, brown fat can break down sugars and fats to warm us up, a process that also consumes excess nutrients. In fact, research supported by the NIH has shown that cold temperatures stimulate brown fat to soak up and burn fuel molecules, potentially protecting against obesity and diabetes by clearing fats and sugars from the bloodstream. Most of our daily activities, from walking up stairs to thinking, rely on mitochondria working properly. But if mitochondria falter, cells can’t use energy well – and that can contribute to common health issues. Studies have linked mitochondrial dysfunction to metabolic disorders (like obesity and type 2 diabetes) and even the aging process itself, since our cells become less efficient as we get older.

Microproteins: Hidden Regulators of Health: The term “microprotein” refers to a protein so small that scientists historically overlooked it. Our genes encode many large proteins, but embedded within some genes are tiny open reading frames that can produce microproteins – miniature proteins just a few dozen amino acids long. For years, these microproteins were dismissed as genetic “junk” or background noise. However, cutting-edge genomics has started to reveal that many microproteins do exist and have important jobs. “Microproteins have long been dismissed as random genetic junk, but our work shows that many are actually crucial regulators of cell physiology,” explains Alan Saghatelian, PhD, a professor at the Salk Institute and senior author of the new study. In recent years, scientists have identified microproteins involved in metabolism, stress responses, and other vital cellular functions. This represents a paradigm shift – even tiny proteins can wield big influence in biology. (The importance of metabolism in health is highlighted in resources like The Secret Life of Fat by biochemist Sylvia Tara, which explains how our fat tissue – including energy-burning brown fat – acts as an active organ, not just passive padding.)

A New Guardian of Metabolic Health: In the Salk Institute study, researchers focused on a microprotein named SLC35A4-MP, which they discovered hidden in the genetic code of a cell’s messenger RNA in 2024. This microprotein resides within the membranes of mitochondria in brown fat cells. To figure out what SLC35A4-MP does, the team conducted experiments in mice. Dr. Andréa L. Rocha, the study’s first author and a postdoctoral researcher in Saghatelian’s lab, helped engineer mice that lacked the gene for this microprotein specifically in their brown fat tissue. The result? Without SLC35A4-MP, the mice’s brown fat cells struggled mightily when put under stress.

The researchers exposed these mice to cold temperatures and a high-fat diet – two challenges that normally make brown fat ramp up its energy-burning metabolism. But mice missing the microprotein could not boost their metabolism in the cold. Their mitochondria became abnormally enlarged, structurally damaged, and inflamed. “We found that SLC35A4-MP regulates mitochondrial function and lipid metabolism in mice,” says Dr. Rocha, “which shows that microproteins cannot be overlooked as we search for factors that regulate health.” In other words, this tiny protein acted like a guardian for the cell’s powerhouses. Without it, not only did the mitochondria break down, but the brown fat cells showed signs of metabolic decline similar to what is seen in obesity – including cellular stress and inflammation. These issues in turn can lead to poorer energy burning and weight gain. The discovery of SLC35A4-MP’s role means scientists have identified a new leverage point in the cell’s machinery that keeps metabolism running smoothly.

Why It Matters – Fighting Obesity and Aging: Obesity and aging are two massive challenges for public health worldwide. According to the World Health Organization, as of 2022 about 43% of adults were overweight and 16% were obese – a prevalence that has more than doubled since 1990. Excess body fat raises the risk of heart disease, diabetes, and other problems. At the same time, our society is getting older: by 2030, 1 in 6 people on the planet will be over 60 years old. Aging is associated with a slowdown in metabolism and a decline in mitochondrial function, contributing to fatigue, muscle loss, and increased susceptibility to chronic diseases. Finding ways to improve mitochondrial health is therefore a priority for extending healthy lifespan. (For a deeper dive into the science of aging, Harvard geneticist David A. Sinclair’s book Lifespan: Why We Age—and Why We Don’t Have To explores cutting-edge insights on how we might slow aging at the cellular level.)

The new discovery of microprotein SLC35A4-MP is exciting because it points to a novel target for interventions. If a small protein can have such a big effect on metabolic fitness in cells, future therapies might be designed to boost its activity – or mimic its effects – in people. “This microprotein is preserving mitochondrial structure and function in brown fat, which is key for maintaining body temperature and energy balance,” notes Dr. Saghatelian. Enhancing mitochondrial resilience could potentially help treat metabolic disorders like obesity, or even mitigate aspects of aging. Of course, it’s early-stage research (done in mice), so any human applications will require much more study. Yet the principle is promising: by leveraging the body’s own tiny molecular tools, we might improve health in ways traditional approaches haven’t achieved. Importantly, this study adds to growing evidence that microproteins in general are an untapped wellspring of biological insight. “Our study says yes, microproteins are important physiological regulators,” Dr. Saghatelian emphasizes. He hopes these findings “add more fuel to the study of microproteins” – suggesting that many more helpful microproteins remain to be discovered for various conditions.

Everyday Health Implications: While scientists work on translating these findings into therapies, there are already practical steps we can take to support our mitochondrial and metabolic health. Decades of public health research have shown that lifestyle factors profoundly influence how well our metabolism functions:

Stay Active: Regular physical activity is one of the best ways to boost your mitochondria. Health agencies like the CDC recommend at least 150 minutes of moderate exercise per week (such as brisk walking) for adults. Exercise encourages your cells to produce more mitochondria and improves the efficiency of existing ones. This helps your body burn calories and may ward off metabolic problems – in fact, being active lowers the risk of developing type 2 diabetes and metabolic syndrome.
Eat a Balanced, Nutritious Diet: What we eat provides the raw materials for our mitochondria. Emphasize whole foods – vegetables, fruits, lean proteins, whole grains, and healthy fats – which contain vitamins and antioxidants that support cell function. Avoid excessive intake of sugary or ultra-processed foods that can contribute to weight gain and inflammation. A moderate calorie intake aligned with your energy needs helps prevent overloading your mitochondria.
Prioritize Sleep and Manage Stress: Poor sleep and chronic stress can disrupt hormones and metabolism. Aim for 7–9 hours of quality sleep per night, and use stress-reduction techniques (like mindfulness or exercise) to keep stress hormones in check. Good sleep and lower stress levels enable mitochondria and other systems to repair and operate optimally, aiding in weight management and healthy aging.
Engage Your Brown Fat (Sensibly): Brown fat is stimulated by cold exposure – that’s why you shiver in a chilly room as brown fat burns fuel to make heat. Some research suggests that safely exposing yourself to cool temperatures (for example, taking a brisk walk on a cool day or a brief cold shower if approved by your doctor) might activate brown fat and slightly boost metabolism. While this isn’t a weight loss cure-all, it highlights how our environment can tweak our biology. Always practice caution and moderation with cold exposure.

By minding these everyday habits, you can help keep your cellular “engines” in shape. As science advances, we may eventually have new tools – like microprotein-based medications – to further enhance metabolic health. It’s intriguing to imagine a future treatment that, say, increases the levels or activity of a beneficial microprotein like SLC35A4-MP to combat obesity or energize aging cells. Entire books have been written about the central role of mitochondria in health and disease (for instance, Mitochondria and the Future of Medicine by Dr. Lee Know illustrates how mitochondrial dysfunction underlies many chronic illnesses). This new research adds a valuable piece to that puzzle by showing that preserving mitochondrial integrity – even through a tiny protein – can have big effects.

Looking Ahead: The discovery of SLC35A4-MP is part of a broader scientific movement toward understanding how small players in our cells affect the bigger picture of health. What other microproteins might be quietly influencing processes like appetite, muscle strength, or brain aging? Uncovering those could open entirely new avenues for preventing disease. The Salk Institute team is optimistic, noting that microprotein research is “springing to life” after years of being underestimated.

For now, this study offers a hopeful message: even the tiniest components of our biology can be harnessed to improve well-being. By blending insights from molecular biology with practical health measures, we move closer to a future where obesity, diabetes, and perhaps certain aspects of aging become more manageable. It’s a potent reminder that in science – as in health – sometimes small changes can make a big difference.

Helpful resources:

1. Power, sex, and suicide: Mitochondria and meaning of life.

2. MG Mitochondrial Supplements with ATP, Vitamins, CoQ10 & PQQ.

Staying Active Boosts Longevity and Gene Health

noreply@blogger.com (Unknown) — Tue, 02 Sep 2025 01:33:00 +0000

A large systematic review published in the British Journal of Sports Medicine pooled data from 85 studies and found that adults who consistently maintain physical activity are about 30–40 % less likely to die from any cause than those who remain inactive. Even people who increase their activity from below recommended levels enjoy a 20–25 % reduction in mortality risk, and switching from a sedentary lifestyle to an active one at any point in adulthood still offers meaningful benefits. The protective effect is more pronounced for cardiovascular disease than for cancer. Researchers stress that current guidelines—150–300 minutes of moderate or 75–150 minutes of vigorous exercise per week—are evidence-based, yet even smaller amounts of movement are better than none.

Beyond lowering mortality risk, physical activity protects nearly every system in the body. The World Health Organization notes that regular activity helps prevent and manage cardiovascular disease, diabetes and some cancers, reduces symptoms of depression and anxiety, enhances brain health and overall well-being, and contributes to healthy growth and development in children and adolescents. Insufficient activity increases the risk of death by 20–30 % and contributes to a growing global burden of noncommunicable diseases. Worryingly, 31 % of adults and 80 % of adolescents worldwide fail to meet recommended activity levels. Sedentary behaviours, such as prolonged sitting or screen time, are linked to higher rates of cardiovascular disease, cancer and type‑2 diabetes.

Emerging science also shows that exercise influences health at the molecular level. A study of identical twins by Washington State University found that siblings who exercised more than 150 minutes per week displayed epigenetic modifications—changes in DNA methylation—linked to lower body mass index and reduced metabolic disease risk. Since the twins share the same DNA, these differences highlight how lifestyle behaviours like physical activity can alter gene expression through epigenetic mechanisms. Such changes may partially explain why regular exercise reduces risk for obesity, type‑2 diabetes and cardiovascular disease.

Researcher Credentials

Author collective – Researchers from multiple international institutions conducted the meta-analysis on physical activity patterns and mortality.
World Health Organization (WHO) – Provides global guidelines and statistics on physical activity and sedentary behaviour.
Dr. Michael Skinner – Biologist at Washington State University; corresponding author on a twin study showing exercise-induced epigenetic changes.
Glen Duncan – Professor and Registry Director at Washington State University; oversaw data collection for the twin study.

Recommended Resources
Explore these products to support an active lifestyle and learn more about exercise science:

Spark: The Revolutionary New Science of Exercise and the Brain – John J. Ratey explains how physical activity transforms brain function and mood.

Cellular Stress Relief: How mRNAs Avoid Traffic Jams During Crises

noreply@blogger.com (Unknown) — Mon, 01 Sep 2025 03:28:00 +0000

When cells face heat, toxins or other challenges, they temporarily shut down most protein production. Ribosomes detach from RNA, and these unprotected RNA strands condense into stress granules—tiny holding areas until conditions improve. Yet some messenger RNAs (mRNAs) must keep working to help cells survive. Researchers at the University of Michigan discovered that these “rescue” mRNAs stay out of stress granules by hanging onto ribosomes via short upstream open reading frames (uORFs), special sequences at the start of the mRNA. Even a single ribosome bound to an mRNA is enough to prevent it from becoming trapped.

The team used chemical inhibitors, single-molecule imaging and engineered RNA reporters to show that removing these uORFs caused mRNAs to lose ribosome association and end up in stress granules. By acting like a molecular “on‑ramp” for ribosomes, uORFs ensure that essential proteins can still be made during a crisis. This insight may inform future strategies for diseases such as ALS and cancer, where stress granule dynamics go awry.

Researcher Credentials

Dr. Stephanie Moon – Assistant professor of Human Genetics at the University of Michigan Medical School; studies how cells respond to stress.
Noah Helton – Ph.D. candidate and first author of the study.
Benjamin Dodd, Ph.D. – Co‑author who contributed insights on ribosome‑mRNA interactions.

Recommended Resources
These items can help deepen your understanding of cellular health and provide tools for managing stress:

The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer – explores how lifestyle choices influence cellular aging and resilience.
Gaiam Restore Hand Therapy Kit – a set of stress‑relief balls designed to improve hand strength and reduce tension.
Molecular Model Kit for Biochemistry – an educational kit to build and visualize RNA, DNA and protein structures.

Timing Your Diet: How Genes and Food Interact to Shape Your Body’s Clock

noreply@blogger.com (Unknown) — Mon, 01 Sep 2025 03:19:00 +0000

Researchers at Baylor College of Medicine have uncovered how your genetic makeup and what you eat work together to influence the liver’s daily rhythms. While the circadian clock is known to regulate sleep and metabolism, the new study finds that diet can reshape these rhythms by interacting with gene variants. By examining human liver samples and two strains of mice over a 24‑hour cycle and after feeding them high‑fat diets, the team discovered that genetic differences determine when certain genes turn on or off. Thousands of genes showed daily patterns only in individuals with specific variants High‑fat diets altered gene rhythms in unique ways: some genes maintained their rhythms, others lost them, and some gained new ones.

The researchers explored how segments of DNA called enhancers and promoters interact over time and found that more than 80 % of these interactions depend on both genetics and nutrition. They pinpointed ESRRγ, a “noncanonical” clock regulator, as a key player; mice lacking this gene lost many rhythmic connections and displayed disrupted fat metabolism. These findings suggest that the timing of meals and lifestyle interventions could be tailored to an individual’s genetic profile to optimize health.

Researcher Credentials

Dr. Dongyin Guan – Assistant professor of medicine (endocrinology) and molecular and cellular biology at Baylor College of Medicine; member of the Dan L Duncan Comprehensive Cancer Center.
Dr. Ying Chen – Postdoctoral fellow in the Guan lab at Baylor College of Medicine.
Dishu Zhou – Research assistant in the Guan lab at Baylor College of Medicine.

Recommended Resources:

Understanding Hyperuricemia: Lifestyle and Molecular Factors Behind High Uric Acid

noreply@blogger.com (Unknown) — Mon, 01 Sep 2025 02:50:00 +0000

Hyperuricemia occurs when the body accumulates too much uric acid because humans lack the enzyme uricase, which normally breaks down purines. A recent review led by Weizheng Zhang explains that high uric acid can develop through a combination of genetic variations (such as differences in genes for uric‑acid transporters and enzymes) and lifestyle factors. Purine‑rich foods (organ meats, red meat, some seafood and beer), obesity, impaired kidney function and dehydration all contribute to this imbalance. When excess uric acid crystallizes, it can trigger gout and raise the risk of cardiovascular disease, metabolic syndrome and kidney problems.

The review highlights that lifestyle changes are central to preventing and managing hyperuricemia. Dietary adjustments—such as reducing intake of purine‑dense foods, alcohol and sugar‑sweetened beverages—lower uric‑acid production, while a diet rich in fruits, vegetables and whole grains supports overall metabolic health. Moderate exercise helps with weight management and insulin sensitivity, but intense workouts can temporarily raise uric‑acid levels. Good hydration dilutes uric acid and promotes its excretion, and adequate sleep and stress management further support metabolic balance.

On the molecular side, variations in genes that encode uric‑acid transporters (SLC2A9, ABCG2) and enzymes such as xanthine oxidase can make some individuals more susceptible to hyperuricemia. Emerging research suggests that the gut microbiome plays a role in uric‑acid metabolism, hinting that probiotics or fiber‑rich diets may help regulate levels. Advances in imaging and omics technologies offer more precise diagnostic tools and may enable personalized treatments in the future, but for now, the cornerstone of care remains holistic lifestyle modification.

Researcher Profile

Weizheng Zhang – Researcher and author of the review; Victorian Infectious Diseases Reference Laboratory (VIDRL), The Peter Doherty Institute, Melbourne, Australia

Recommended Resources
Here are a few products related to gout, uric‑acid management and healthy living:

Low‑Purine Diet Cookbook: Recipes for Managing Gout and Hyperuricemia – a guide to delicious meals that minimize purine intake: Read here.
Insulated Water Bottle (32 oz) for Daily Hydration – staying hydrated helps dilute uric acid and support kidney function: Get it here.
Understanding Gout: A Comprehensive Guide to Managing Uric Acid Levels – an accessible book covering causes, lifestyle strategies and long‑term management: Read here.

Balancing Sweetness and Longevity: How Eating Well and Cutting Sugar May Keep Cells Younger

noreply@blogger.com (Unknown) — Mon, 01 Sep 2025 02:30:00 +0000

Researchers working with a cohort of 342 midlife women in Northern California investigated how diet quality relates to biological age at the cellular level. Each participant logged what she ate and provided a saliva sample. The samples were analyzed with an “epigenetic clock,” a molecular test that measures chemical marks on DNA associated with aging. Diets rich in fruit, vegetables, whole grains and other antioxidant‑packed foods – patterns similar to the Mediterranean and other anti‑inflammatory diets – were linked with lower epigenetic. In other words, cells looked “younger” when people followed nutrient‑dense eating habits.

A key finding was the role of added sugar. Even among people with otherwise healthy diets, each extra gram of added sugar correlated with a slightly older biological age. Study co‑senior author Elissa Epel, a professor of psychiatry at the University of California, San Francisco, noted that excessive sugar intake accelerates molecular aging and undermines healthy longevity. The team estimated that cutting 10 grams of added sugar per day – about the amount in half a chocolate bar or a quarter of a can of cola – could shave roughly 2.4 months off one’s biological age over time. Lead researcher Dorothy Chiu, a postdoctoral scholar at the UCSF Osher Center for Integrative Health, emphasized that following established nutritional guidelines “may promote a younger cellular age relative to chronological age”.

These insights underline how lifestyle choices can influence gene regulation and DNA maintenance. The researchers created an “Epigenetic Nutrient Index” highlighting vitamins and minerals (including vitamins A, C, B12 and E, folate, selenium and magnesium) that support DNA repair. Emphasizing these nutrients – while limiting processed sugar – offers a practical way to support healthy aging through everyday meals.

Researcher Credentials

Dorothy Chiu, PhD – Postdoctoral scholar, UCSF Osher Center for Integrative Health (first author)
Elissa Epel, PhD – Professor of Psychiatry and Behavioral Sciences, University of California, San Francisco
Barbara Laraia, PhD, RD – Professor in the Food, Nutrition and Population Health program, University of California, Berkeley
Elissa Hamlat, PhD – Co‑author, University of California, San Francisco
Joshua Zhang, PhD – Co‑author, University of California, Los Angeles

Recommended Resources
If you’re interested in exploring healthy eating and its molecular effects, these products might be helpful:

The Complete Mediterranean Cookbook: 500 Vibrant, Kitchen‑Tested Recipes for Living and Eating Well Every Day – A comprehensive guide to nutrient‑dense meals inspired by the Mediterranean diet: Read here.
Sugar Detox: A 21‑Day Sugar Detox Program to Reset and Break Sugar Addiction – Practical strategies for reducing added sugar intake and improving overall health: Read here.
The Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease, and Inheritance – An accessible introduction to how lifestyle and environment shape gene expression: Read here.

Microprotein SLC35A4‑MP: a tiny regulator of mitochondrial health

noreply@blogger.com (Unknown) — Sun, 31 Aug 2025 17:31:00 +0000

Tiny proteins hidden in our genetic code are changing the way scientists think about cell biology. A research team from the Salk Institute recently reported that a newly discovered microprotein, SLC35A4‑MP, helps maintain the structure and function of mitochondria – the energy‑producing “powerhouses” of our cells. Microproteins like SLC35A4‑MP are encoded in sections of messenger RNA that were once dismissed as non‑coding junk. As analytical techniques improved, researchers realized these regions can encode functional proteins that influence metabolism and stress responses.

Why it matters

Mitochondria convert nutrients into energy, regulate body temperature and help maintain metabolic balance. When mitochondrial function declines, metabolic diseases such as obesity and age‑related disorders can follow. In the Salk study, researchers focused on brown fat—a metabolically demanding tissue that generates heat. They removed the gene encoding SLC35A4‑MP from brown fat cells in mice and subjected the animals to cold exposure or a high‑fat diet. Without the microprotein, the animals could not increase their metabolism when cold, and their mitochondria were enlarged, structurally disorganized and inflamed. These defects extended beyond the organelle: the cells showed signs of remodeling and inflammation similar to what is seen in obesity‑related conditions.

The findings show that SLC35A4‑MP plays a fundamental role in regulating mitochondrial stress responses. Because mitochondria are found in every cell type, this microprotein may become a therapeutic target for diseases involving metabolic and mitochondrial dysfunction, ranging from obesity to aging.

Key points from the study

Discovery of SLC35A4‑MP: Senior author Alan Saghatelian, a professor and Dr. Frederik Paulsen Chair at the Salk Institute, and his colleagues discovered the genetic code for SLC35A4‑MP in 2024 within an upstream open reading frame on a messenger RNA strand. Upstream reading frames were once thought to be non‑coding, but new sequencing and ribosome‑profiling methods showed that they can encode functional microproteins.
Physiological role in mice: To test whether SLC35A4‑MP has a biological role, the team generated mice lacking the microprotein in brown fat. These mice could not properly regulate their metabolism during cold exposure, and their mitochondria showed structural damage, inflammation and an inability to adjust to metabolic stress.
Implications for health: By preserving mitochondrial structure and helping brown fat respond to metabolic stress, SLC35A4‑MP may support metabolic health. The researchers suggest that microprotein‑based therapies could eventually help treat obesity, aging and other mitochondrial disorders.

Researchers involved

Alan Saghatelian, PhD – Professor and Dr. Frederik Paulsen Chair at the Salk Institute; senior author and microprotein specialist.
Andréa Rocha, PhD – Postdoctoral researcher in Saghatelian’s lab and first author; she conducted the functional experiments in mice.
Additional team members: Antonio Pinto, Jolene Diedrich, Huanqi Shan, Eduardo Vieira de Souza, Joan Vaughan and Mark Foster (Salk Institute); Christian Schmedt (Novartis Research Foundation and Integrate Bioscience); Guy Perksin and Mark Ellisman (UC San Diego); Kaja Plucińska and Paul Cohen (Rockefeller University); and Srinath Sampath (Novartis Research Foundation and UC San Diego).

Related books and resources:

To delve deeper into mitochondrial biology and health, here are some relevant books. These direct links include your Amazon Associates ID:

Mitochondria and the Future of Medicine by Lee Know
Power, Sex, Suicide: Mitochondria and the Meaning of Life by Nick Lane
Good Energy: The Surprising Connection Between Metabolism and Limitless Health by Casey Means

Rethinking Cannabis: Unlocking the Genetic Blueprint of an Ancient Powerhouse

noreply@blogger.com (Unknown) — Sun, 01 Jun 2025 12:21:00 +0000

Cannabis has played a critical role in human societies for over ten millennia. Although contemporary attention often centers on its psychoactive component, THC (tetrahydrocannabinol), historically this plant served as an essential source of seed oil, textiles, and nourishment. Despite its longstanding significance, cannabis remains relatively underexplored and underexploited in modern agriculture. Recent legislative changes in the United States—most notably the 2014 and 2018 Farm Bills—have spurred renewed interest in cultivating cannabis for medicinal, grain, and fiber purposes.

A team at the Salk Institute has now produced the most exhaustive and precise genetic atlas of cannabis to date. By examining 193 distinct cannabis genomes, researchers uncovered remarkable genetic diversity and complexity within this foundational crop. This collaborative effort involved Oregon CBD, Oregon State University, and the HudsonAlpha Institute for Biotechnology, and culminated in findings published in Nature on May 28, 2025. These discoveries promise to catalyze significant advances in cannabis-based agriculture, medicine, and industry.

“Cannabis is one of the most extraordinary plants on Earth. Despite its global importance as a source of medicine, food, seed oil, and fiber for at least the last 10,000 years, it remains one of the least developed major crops of modern times, largely due to a century of legal restrictions,” says Todd Michael, senior author of the study and research professor at Salk. “Our team constructed the most complete genetic map, or pangenome, of the plant to date by analyzing nearly 200 diverse cannabis genomes, showing that we are just starting to see the full potential of this amazing plant. Those same legal restrictions spurred an underground breeding revolution, revealing cannabis’s power as a chemical factory. With this new genomic blueprint, we can now apply modern breeding to unlock novel compounds and traits across agriculture, medicine, and biotechnology.”

Background: Cannabis as a Versatile Crop

Cannabis sativa, often referred to as hemp, is a flowering species indigenous to Asia. Its versatility stemmed from unique characteristics—such as fiber strength suitable for textiles and the capacity to produce high concentrations of cannabinoids—that made it indispensable through much of human history. Today’s researchers envision cannabis oil eventually rivaling conventional seed oils like canola or soybean, and anticipate that cannabis-derived compounds might even serve as sustainable alternatives to fossil fuels.

Often described as a “chemical powerhouse,” cannabis can allocate over 30 percent of its dry biomass to terpenes and cannabinoids. These small molecules play defensive roles against pests in the field, yet humans have repurposed them for their aromatic and therapeutic properties. Terpenes are responsible for the distinctive fragrances of fruits and flowers, while cannabinoids interact with the endocannabinoid system in humans, delivering a range of effects. The strain “Charlotte’s Web,” rich in cannabidiol (CBD), brought widespread attention to cannabis’s medicinal potential when it alleviated epileptic seizures in children. Beyond CBD and THC, more than one hundred lesser-known cannabinoids are under investigation for treating conditions such as chronic pain, arthritis, nausea, asthma, depression, and anxiety.

Historically, breeding efforts—often conducted clandestinely because of legal restrictions—have dramatically shaped cannabis’s chemical profile. However, until now, the impact of this selective breeding on the plant’s overall genetic diversity remained poorly understood. Two primary challenges have hampered comprehensive genetic insight: first, cannabis is among the minority of flowering plants that exhibit dioecy (separate male and female plants); second, its genome is replete with transposable elements—repetitive DNA segments capable of relocating within the genome—which complicate sequencing and assembly efforts.

Key Discoveries: Unprecedented Genetic Diversity

To map cannabis’s genetic architecture, the Salk team employed both short-read and long-read DNA sequencing technologies. Traditional short-read methods fragment DNA into small stretches (hundreds of base pairs), making it difficult to reconstruct complex or repetitive regions. In contrast, long-read sequencing captures thousands of base pairs in a single read, allowing for more accurate assembly of difficult genomic regions.

“There are limits to what you can discover with short-read sequencing technologies, since those short genetic excerpts are impossible to stitch together in any meaningful way when looking at complex regions of the genome, especially repetitive DNA sequences,” explains co–first author Lillian Padgitt-Cobb, a postdoctoral researcher in Michael’s lab. “We’re among the first to harness this long-read technology at scale in the pangenome context, and with that comes all these insights into structural variation and gene ordering that can inform end-game decisions about breeding favorable traits into cannabis plants.”

This investigation builds upon earlier work: in 2018, Todd Michael generated the first chromosome-level cannabis genome using long-read sequencing, elucidating the loci responsible for cannabinoid biosynthesis and clarifying the breeding origins of the “Charlotte’s Web” variety. The current study, however, extends far beyond a single reference assembly. By assembling 193 genomes—drawn from 144 individual plants worldwide, with haplotype resolution for each—researchers achieved a far more comprehensive “pangenome.” Because cannabis is diploid (possessing two chromosome sets, one maternal and one paternal), haplotype resolution meant that each plant contributed two separate genome assemblies—amounting to 193 total genomes.

Resolving both haplotypes for each individual plant revealed an extraordinary degree of variation: in some regions, cannabis exhibits up to twenty times more genetic diversity than humans. This level of resolution allowed the team to trace exactly which chromosomal segments were inherited from each parent, providing direct insight into breeding histories and genetic backgrounds.

Gene Presence and Variation

Analysis of the pangenome revealed that:

23 percent of genes are found in every genome assembly (core genes).
55 percent of genes appear in 95 to 99 percent of genomes (near-universal genes).
21 percent fall within a group present in 5 to 94 percent of genomes (variable genes).
Fewer than 1 percent are unique to a single genome.

Interestingly, genes involved in cannabinoid biosynthesis tended to be highly conserved across varieties, reflecting intense human-driven selection for THC and CBD content. Conversely, genes linked to fatty acid metabolism, growth, and defense exhibited substantial variability—presenting opportunities for breeders to develop hemp with improved field performance or enhanced nutritional profiles in hemp oil. Notably, the study identified structural variants in fatty acid biosynthesis genes that influence production of tetrahydrocannabivarin (THCV), a less common cannabinoid noted for its non‑psychoactive, energizing properties.

Further investigation showed that both THC acid synthase (THCAS) and CBD acid synthase (CBDAS) genes are under strong selective pressure in cultivated varieties, explaining the uniformity of cannabinoid content in many commercial lines. These synthase genes, and other cannabinoid-related loci, often reside within transposable elements—mobile genetic sequences that can jump to new genomic locations. Breeding programs targeting genes embedded in these transposons have unintentionally generated a wealth of structural variation, contributing to the remarkable phenotypic diversity seen in modern cannabis.

Sex Chromosome Insights

Because cannabis is dioecious, understanding its sex chromosomes is critical. Previous reference genomes lacked full data on both X and Y chromosomes, leaving male-specific genes unexplored. By including sex chromosomes in their assemblies, the Salk team produced the first comprehensive view of the cannabis Y chromosome. Among their findings, they discovered male-only genes that offer pathways to breed offspring with enhanced agronomic traits. Until now, many marijuana breeders have practiced “feminization” (inducing female plants to produce pollen), thereby bypassing the Y chromosome entirely and potentially overlooking valuable genetic diversity unique to male plants.

Looking Ahead: Breeding for Health, Industry, and Sustainability

Armed with this expansive pangenome, researchers and breeders can pursue a variety of objectives:

Identification of Wild Relatives: By comparing European and Asian hemp genomes, the team suspects the existence of an ancient, as-yet-undiscovered wild relative in Asia. Such a wild lineage is likely to harbor unique adaptations—drought tolerance, disease resistance, or distinctive metabolic profiles—that breeders could harness to develop more resilient cultivars.
Reintegration of Male Genetics: Given the newly characterized Y chromosome, breeding strategies that include true male plants could unlock untapped trait potential. Male‑specific genes may contribute to higher yields, enhanced fiber quality, or unique cannabinoid profiles. Including male genetics could augment breeding programs that have traditionally focused solely on female lines.
Improved Nutritional Profiles: Variable genes affecting fatty acid metabolism offer a promising route to optimize hemp seed oil composition. By selectively breeding favorable alleles, hemp oil could become competitive with established seed oils—such as canola or soybean—or even outperform them nutritionally.
Expanded Medicinal Uses: Insights into cannabinoid synthase clusters and their genomic context may enable breeders to develop novel chemotypes—plants producing tailored ratios of cannabinoids and terpenes for specific therapeutic applications. For example, varieties engineered to overproduce THCV could address metabolic disorders, while lines optimized for minor cannabinoids might target neuroinflammatory or psychiatric conditions.
Industrial Hemp Optimization: Variable genes associated with growth and defense can be selected to produce hemp varieties suited to diverse climates and soil types. Improved fiber strength, pathogen resistance, or biomass yield could expand hemp’s role in textiles, bioplastics, and construction materials.

“Over the last 10 years, breeders have already done a decent job of getting yields up and making cannabis an economically viable crop,” says co–first author Ryan Lynch, a postdoctoral researcher in Michael’s lab. “Once there’s market interest there, paired with these new insights into cannabis genomes that can guide breeding efforts, I can see hemp and hemp oils really booming in both human health and industry applications.”

Try Hemp gummies from Amazon.

In the near term, the pangenome will serve as an open-access resource for scientists worldwide, guiding crop‑improvement strategies and accelerating discovery. By tapping into previously hidden genetic variation, researchers can unlock cannabis’s full potential—as a high‑yield fiber crop, a nutrient‑rich oilseed, and a source of novel medicinal compounds.

Acknowledgments and Funding

Additional authors on the paper include Nolan Hartwick, Nicholas Allsing, Anthony Aylward, Allen Mamerto, Justine Kitony, Kelly Colt, Emily Murray, Tiffany Duong, and Heidi Chen (Salk Institute); Andrea Garfinkel, Aaron Trippe, and Seth Crawford (Oregon CBD); Brian Knaus and Kelly Vining (Oregon State University); and Philip Bentz, Sarah Carey, and Alex Harkess (HudsonAlpha Institute for Biotechnology).

Funding for this work was provided by the Tang Genomics Fund; the National Science Foundation (NSF‑IOS PRFB 2209290, IOS‑PGRP CAREER 2236530); the Bill & Melinda Gates Foundation (INV‑040541); and the U.S. Department of Agriculture (USDA NIFA 2022‑67012‑38987, USDA NIFA 2023‑67013‑39620).

About the Salk Institute for Biological Studies

The Salk Institute is committed to uncovering life’s fundamental mechanisms. Founded by Jonas Salk—developer of the first safe and effective polio vaccine—the Institute is a nonprofit, independent research organization dedicated to breakthroughs in neuroscience, cancer, aging, immunobiology, plant biology, and computational biology. Small by choice and intimate by design, Salk’s world‑class scientists pursue fearless research aimed at improving human health and well‑being. For more information, visit www.salk.edu. Journal: Nature.

Burkitt Lymphoma Development Linked to Malaria Infection, Research Shows

noreply@blogger.com (Unknown) — Wed, 21 May 2025 01:54:00 +0000

Recent research published in The Journal of Immunology has revealed important insights into how Plasmodium falciparum infection, which causes malaria, contributes to the development of Burkitt lymphoma (BL). This finding helps explain why BL is the most prevalent childhood cancer in equatorial Africa and New Guinea.

Long-Standing Connection Finally Explained

Scientists have recognized an association between BL and P. falciparum malaria since the late 1950s, but until now, researchers couldn't explain the biological mechanism behind this connection.

"The discovery that malaria directly increases childhood cancer risk suggests that efforts to reduce P. falciparum malaria in Africa could simultaneously decrease Burkitt lymphoma cases," explained the study's lead researcher, Dr. Rosemary Rochford from the University of Colorado Anschutz School of Medicine, where she serves as Distinguished Professor of Immunology and Microbiology.

Cancer of the Immune System

Burkitt lymphoma affects B cells, which are critical immune system components responsible for antibody production. While BL remains rare worldwide, its frequency is ten times higher in regions where P. falciparum malaria is endemic. Notably, although humans can contract malaria from five different Plasmodium species, only P. falciparum shows this strong association with Burkitt lymphoma.

Enzyme Activity Reveals the Link

The researchers discovered significantly increased levels of an enzyme called activation-induced cytidine deaminase (AID) in B cells of children infected with P. falciparum malaria. This finding is particularly significant because AID plays a crucial role in BL development.

One characteristic feature of Burkitt lymphoma is the translocation of the MYC gene—a genetic abnormality where DNA breaks away from one chromosome and attaches to another. Since AID is essential for this MYC translocation process, its elevated presence in malaria patients provides strong evidence of P. falciparum's role in causing BL.

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Study Methodology and Findings

The research team compared blood samples from children with uncomplicated malaria (characterized by non-specific symptoms like fever, chills, headache, and nausea without severe organ dysfunction) to samples from children without malaria. Their analysis revealed that AID was not only significantly elevated in the B cells of children with uncomplicated malaria but was also fully functional—further supporting P. falciparum's role in BL development.

Future Research Directions

"We hope this study contributes to the growing evidence highlighting AID's critical role in Burkitt lymphoma etiology and potentially in other non-Hodgkin's lymphomas," noted Dr. Rochford.

Her team continues to investigate other effects of P. falciparum on children's immune function and how these changes create conditions favorable for cancer development.

Access to Research

The complete research article can be found in The Journal of Immunology or through AAI News. Those interested in obtaining a PDF copy of the research can contact the American Association of Immunologists.

About The American Association of Immunologists

The American Association of Immunologists (AAI) represents one of the world's largest communities of immunologists and scientists in related fields. The organization aims to enhance global health and well-being by advancing immunology and increasing public understanding of the immune system. AAI members have contributed to many significant biomedical breakthroughs of the past century, including cancer immunotherapies, antibody treatments, transplantation technologies, and vaccine development. The association supports immunology researchers through knowledge dissemination, community building, advocacy, and public education.

About The Journal of Immunology

The Journal of Immunology publishes peer-reviewed research describing new findings across all experimental immunology areas, encompassing both basic and clinical research. The journal is owned by the American Association of Immunologists and published in partnership with Oxford University Press.

Related Studies:

CRISPR Beyond Gene Editing: Novel Bacterial Immunity Mechanisms Revealed

noreply@blogger.com (Unknown) — Sat, 17 May 2025 22:24:00 +0000

Bacteria employ sophisticated defensive strategies against viral threats, with CRISPR-based immunity systems standing at the forefront of microbial protection mechanisms. Recent research has uncovered an innovative component of these systems called Cat1, which demonstrates remarkable complexity in its approach to cellular defense.

Advanced CRISPR Immunity Mechanisms

While CRISPR-Cas9 has gained fame as a revolutionary genetic editing tool, scientists continue to discover that bacterial CRISPR systems utilize multiple defensive strategies beyond the well-known "genetic scissors" approach. Researchers at the Laboratory of Bacteriology and the Structural Biology Laboratory have been investigating specialized immune components called CARF effectors, which represent cutting-edge developments in our understanding of microbial immunity.

These CARF effectors function as defensive weapons within CRISPR systems, each employing distinct methods to achieve a common goal: halting cellular activity to prevent viral proliferation throughout bacterial populations.

Cat1: A Newly Discovered Defense Mechanism

The newest identified CARF effector, designated Cat1, demonstrates an extraordinarily complex molecular structure that allows it to deplete NAD+, a metabolite essential for cellular function. This depletion effectively removes the necessary fuel for viral replication, bringing invasions to a standstill.

"The collective work of our labs is revealing just how effective—and different—these CARF effectors are," notes the lead researcher. "The range of their molecular activities is quite amazing."

How CRISPR Systems Defend Bacteria

CRISPR represents a mechanism within the adaptive immune systems of bacteria and certain single-cell organisms that provides protection against viruses known as phages. Six types of CRISPR systems have been identified, all following a similar operational principle: CRISPR RNA identifies foreign genetic material, triggering a cas enzyme to mediate an immune response.

Growing evidence suggests that CRISPR systems deploy diverse defensive strategies beyond basic genetic editing. CARF effector immunity appears to function by creating environments inhospitable to viral replication. For instance, the previously discovered Cam1 CARF effector causes membrane depolarization in infected cells, while Cad1 triggers a cellular "fumigation" by releasing toxic molecules.

Cat1's Unique Metabolic Defense Strategy

Researchers identified Cat1 using Foldseek, an advanced structural homology search tool. The protein responds to viral presence through binding with secondary messenger molecules called cyclic tetra-adenylate (cA4), which stimulate the enzyme to cleave NAD+.

"Once a sufficient amount of NAD+ is cleaved, the cell enters a growth-arrest state," explains one of the study's co-authors. "With cellular function paused, the phage can no longer propagate and spread to the rest of the bacterial population. In this way, Cat1 provides population-level bacterial immunity."

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Remarkable Structural Complexity

Detailed structural analysis using cryo-EM revealed that Cat1 possesses a surprisingly complex structure. The Cat1 protein forms dimers connected by cA4 signal molecules, creating long filaments upon viral infection that trap NAD+ metabolites within specialized molecular pockets. Once cleaved by these Cat1 filaments, NAD+ becomes unavailable for cellular use.

The protein's structural complexity extends further—the filaments interact to form trigonal spiral bundles, which can expand into pentagonal spiral bundles. The precise purpose of these structural components remains under investigation.

Unlike other CRISPR systems that typically employ multiple activities for immunity, bacteria encoding Cat1 often rely primarily on this single mechanism for their defensive response.

Future Directions in CRISPR Immunity Research

While researchers have established that CARF effectors effectively prevent phage replication, many details about their mechanisms remain to be discovered. "It will be fascinating to see where this work leads us next," notes the lead investigator.

This research expands our understanding of bacterial immune systems and may potentially inform future applications of CRISPR technology beyond gene editing, opening new avenues for biotechnology and therapeutic development.

Journal Science

Pulse rate predicts faster cognitive declines in adults

noreply@blogger.com (Unknown) — Wed, 07 May 2025 23:30:00 +0000

Healthy hearts are adaptable, and heartbeats exhibit complex variation as they adjust to tiny changes in the body and environment. Mass General Brigham researchers have applied a new way to measure the complexity of pulse rates, using data collected through wearable pulse oximetry devices. The new method, published in Journal of the American Heart Association, provides a more detailed peek into heart health than traditional measures, uncovering a link between reduced complexity and future cognitive decline.

“Heart rate complexity is a hallmark of healthy physiology,” said senior author Peng Li, PhD, of the Department of Anesthesia, Critical Care and Pain Medicine at Massachusetts General Hospital (MGH) and the Division of Sleep and Circadian Disorders at Brigham and Women’s Hospital (BWH), both founding members of the Mass General Brigham healthcare system. “Our hearts must balance between spontaneity and adaptability, incorporating internal needs and external stressors.”

The study used data from 503 participants (average age 82, 76% women) in the Rush Memory and Aging Project. The researchers analyzed overnight pulse rate measurements—collected by a fingertip pulse oximetry device known as the Itamar WatchPAT 300 device—and comprehensive measures of cognitive functions, collected around the same time as the pulse rate measurement and at least one annual follow-up visit up to 4.5 years later.

The team found that people with greater complexity in their heartbeats at baseline tend to experience slower cognitive decline over time. They determined that the conventional measures of heart rate variability did not predict this effect, indicating their measure was more sensitive in capturing heart functions predictive of cognitive decline.

The researchers plan to investigate whether pulse rate complexity can predict development of dementia, which would make it useful for identifying people at an early stage who might benefit from therapeutic interventions.

“The findings underscore the usefulness of our approach as a noninvasive measure for how flexible the heart is in responding to nervous system cues,” said lead author Chenlu Gao, PhD, also in the Department of Anesthesia, Critical Care and Pain Medicine at MGH. “It is suitable for future studies aimed at understanding the interplay between heart health and cognitive aging.”

Authorship: In addition to Gao and Li, Mass General Brigham authors include Shahab Haghayegh, Ruixue Cai, Lei Gao, and Kun Hu. Additional authors include Andrew S.P. Lim, Jingyun Yang, Lei Yu, Agustin Ibanez, Aron S. Buchman, and David A. Bennett.

Disclosures: Li has received a monetary gift to support research from iFutureLab, serves on the iFutureLab-HEKA Scientific Advisory Board as the Chair of Cardiac Dynamics and Honorary Life-Time Co-Founder and has received consulting fees, has received honorarium for lecturing from China Pharmaceutical University. Hu serves on the iFutureLab-HEKA Scientific Advisory Board as the Chair of Medical Biodynamics and Honorary Life-Time Co-Founder and has received consulting fees.

Funding: This work was supported by the BrightFocus Foundation (A2020886S). The Rush Memory and Aging Project is supported by NIH (R01AG17917, R01AG052488).

Paper cited: Gao C et al. “Reduced complexity of pulse rate is associated with faster cognitive decline in older adults” Journal of the American Heart Association DOI: 10.1161/JAHA.125.041448

Ultra processed foods speed up Parkinson's disease early symptoms

noreply@blogger.com (Unknown) — Wed, 07 May 2025 23:25:00 +0000

People who eat more ultra processed foods like cold breakfast cereal, cookies and hot dogs are more likely to have early signs of Parkinson’s disease when compared to those who eat very few ultra processed foods, according to a study published in the May 7, 2025, online in Neurology®, the medical journal of the American Academy of Neurology. The study does not prove that eating more ultra processed foods causes early signs of Parkinson’s disease; it only shows an association.

Researchers looked for signs of prodromal Parkinson’s disease, which is the earliest stage, when neurodegeneration begins, but more characteristic symptoms of Parkinson’s disease, like tremors, balance problems and slow movement, have not yet begun. These early symptoms can begin years or even decades before the typical symptoms start.

“Eating a healthy diet is crucial as it has been associated with a lower risk of neurodegenerative diseases and the dietary choices we make today can significantly influence our brain health in the future,” said study author Xiang Gao, MD, PhD, of Institute of Nutrition, Fudan University in Shanghai, China. “There's growing evidence that diet might influence the development of Parkinson's disease. Our research shows that eating too much processed food, like sugary sodas and packaged snacks, might be speeding up early signs of Parkinson's disease.”

The study included 42,853 people with an average age of 48 who did not have Parkinson’s disease at the start of the study. They were followed up to 26 years.

Participants had regular medical exams and completed health questionnaires. Researchers reviewed results to determine if they had early signs of Parkinson’s disease, including rapid eye movement sleep behavior disorder, constipation, depressive symptoms, body pain, impaired color vision, excessive daytime sleepiness and reduced ability to smell.

Participants completed a food diary every two to four years, listing what they ate and how often.

Researchers looked at several types of ultra processed foods including sauces, spreads, or condiments; packaged sweets; snacks or desserts; artificially or sugar-sweetened beverages; animal-based products; yogurt or dairy-based desserts; and packaged savory snacks. One serving was equivalent to a single can of soda, one ounce of potato chips, one slice of packaged cake, a single hot dog or one tablespoon of ketchup.

Researchers calculated how many ultra processed foods participants ate on average per day.

They divided participants into five groups. The highest group ate 11 or more servings of ultra-processed food per day on average. The lowest group ate an average of fewer than three servings per day.

After adjusting for factors such as age, physical activity and smoking, researchers found that participants who ate 11 or more servings of ultra processed foods per day had a 2.5-fold higher likelihood of having three or more early signs of Parkinson’s disease compared to those consuming fewer than three servings per day.

When looking at individual early signs of Parkinson’s disease, researchers also found that eating more ultra processed foods was tied to an increased risk for nearly all symptoms except constipation.

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Choosing to eat fewer processed foods and more whole, nutritious foods could be a good strategy for maintaining brain health,” said Gao. “More studies are needed to confirm our finding that eating less processed food may slow down the earliest signs of Parkinson's disease.”

A limitation of the study was that the amount of ultra processed food consumed was self-reported, so participants may not have remembered accurately how much and what specific foods they ate.

The study was supported by the National Institute of Neurological Disorders and Stroke, the municipal public health system in Shanghai, China, the National Natural Science Foundation of China and the China Postdoctoral Science Foundation.

Discover more about Parkinson’s disease at BrainandLife.org, from the American Academy of Neurology. This resource also offers a magazine, podcast, and books that connect patients, caregivers and anyone interested in brain health with the most trusted information, straight from the world’s leading experts in brain health. Follow Brain & Life® on Facebook, X, and Instagram.

The American Academy of Neurology is the leading voice in brain health. As the world’s largest association of neurologists and neuroscience professionals with more than 40,000 members, the AAN provides access to the latest news, science and research affecting neurology for patients, caregivers, physicians and professionals alike. The AAN’s mission is to enhance member career fulfillment and promote brain health for all. A neurologist is a doctor who specializes in the diagnosis, care and treatment of brain, spinal cord and nervous system diseases such as Alzheimer's disease, stroke, concussion, epilepsy, Parkinson's disease, multiple sclerosis, headache and migraine.

Food allergy risk in infants linked to avocado consumption in pregnant women

noreply@blogger.com (Unknown) — Wed, 07 May 2025 23:18:00 +0000

Journal: Pediatric Research. 10.1038/s41390-025-03968-4

An observational study among 2,272 mother-child pairs in Finland found that infants had 44% lower odds of developing food allergies at 12 months if their mother consumed fresh avocado during pregnancy, after adjusting for other lifestyle, delivery, and maternal health factors.

Decades of research have explored the relationship between maternal diet and allergic outcomes in infants, but this is the first published study to link avocados in the maternal diet to a lower risk of infant food allergies—a growing public health concern that affects nearly one in 13 children, or roughly two in every classroom, according to Food Allergy Research and Education(FARE).

Given food allergy has reached epidemic levels, the Avocado Nutrition Center supported this research to grow the world’s understanding of how avocado, a food with nutrients that support fetal and infant development, may further benefit children.

“As a caregiver, the growing prevalence of food allergy feels very scary and out of my control,” says Sari Hantunen, study author and Senior University Lecturer at the University of Eastern Finland. “There is no cure for food allergy, but promising prevention and therapeutic strategies are in development as well as emerging research such as this. Based on these findings, it’s encouraging to know that eating avocados may provide even more value to maternal and children’s health, beyond the benefits that have already been established through scientific research.”

Researchers analyzed data collected from 2013 to 2022 as part of the Kuopio Birth Cohort (KuBiCo). Avocado intake was assessed using an online food frequency questionnaire during the first and third trimesters. Participants who reported eating any avocado (>0 grams) in either trimester were defined as avocado consumers, and non-consumers were those who did not report consuming any avocado in either trimester.

Infant allergic outcomes, including rhinitis, paroxysmal wheezing, eczema, and food allergy, were evaluated at 12-months of age. After adjusting for factors such as maternal and gestational age at delivery, education, diet quality, smoking, alcohol consumption, BMI in the ﬁrst trimester, and breastfeeding, food allergy was found to be significantly higher in infants of non-avocado consumers (4.2%) versus avocado consumers (2.4%). No associations were found for other allergic conditions when all other factors were considered.

Mothers who consumed avocado during pregnancy tended to be older at delivery, be less likely to undergo a caesarean delivery, be a non-smoker, breastfeed for a longer duration, have higher diet quality scores, and have lower BMI levels in the first trimester.

Findings from this study cannot establish causation or be applied to all audiences, and while more research is needed to understand the exact mechanism, they underscore the value of avocados which provide the following nutrients per serving (1/3 medium avocado):

A good source of fiber, a nutrient most Americans under-consume
A good source of folate, essential for fetal neural and heart development
Lutein (136 mcg), critical for proper eye development in utero
Naturally good fats (mono- and polyunsaturated fats), vital for early structural and functional brain development

The Dietary Guidelines for Americans recommends pregnant women eat 2 ½ to 3 ½ cups of vegetables a day and toddlers aged 12-23 months eat 2/3 - 1 cup per day. One avocado counts as a cup.

About Avocados – Love One Today®

Avocados – Love One Today® is a leading source of the healthiest reasons and tastiest ways to enjoy fresh avocados. A science-based resource, it provides facts about fresh avocados in relevant and credible ways to help make it easy for health professionals and consumers to learn more about the nutritional benefits of fresh avocados and ways to include them in everyday menus. Visit www.LoveOneToday.com for avocado nutrition, recipes, and tips.

Research eases worries that prolonged infections are contributing to the emergence of SARS-CoV-2 variants.

noreply@blogger.com (Unknown) — Tue, 25 Jun 2024 02:59:00 +0000

During the early stages of the pandemic, healthcare professionals observed that certain individuals with compromised immune systems were experiencing persistent SARS-CoV-2 infections, sometimes lasting for weeks or even months. This raised concerns about the potential for a viral variant to emerge that could take advantage of an extended battle with the immune system.

A recent prospective study published in the Lancet Microbe, led by Dr. Adam Lauring from the Division of Infectious Disease at Michigan Medicine, explores which patient populations are at a heightened risk of prolonged infections. This study, part of the CDC-sponsored IVY Network based at Vanderbilt University, closely monitored 150 immunocompromised COVID-19 patients across five U.S. health systems in 2022.

The diverse group of participants included individuals with various immunocompromising conditions, such as those with B-cell cancers or undergoing anti-B cell therapy, solid organ or stem cell transplant recipients, individuals with AIDS, and those with non-B cell cancers and autoimmune or autoinflammatory conditions.

Contrary to initial concerns, the study found that only 25% of patients tested positive using the highly sensitive PCR test for 21 days or more after the onset of illness. Only 8% tested positive for live virus for the same duration, with the median time to the last positive test being nine days.

Notably, individuals with AIDS and those with B-cell cancers were more prone to prolonged infections compared to patients with autoimmune diseases or non-B cell cancers. Among the 59 patients with solid organ transplants under T-cell immunosuppression, only one experienced an infection lasting over 56 days.

The study also highlighted a correlation between extended infections and specific immunosuppressive therapies. Patients undergoing rituximab or CAR-T therapy, which target B cells, exhibited a higher likelihood of enduring infections, underscoring the crucial role of antibodies produced by B cells in immunity.

Importantly, the study found that mutations in patients with prolonged infections rarely matched those of variants circulating globally. Dr. Lauring emphasized that a virus's ability to escape immunity differs between immunocompromised individuals and the general population.

Given the evolving landscape of global immunity through vaccination and infection, monitoring this specific patient population for new variants may not be practical. Nonetheless, the study offers valuable insights into identifying immunocompromised patients at the highest risk. Dr. Lauring hopes that this research will inspire renewed efforts to develop more effective therapies for these vulnerable individuals.

Reference: SARS-CoV-2 shedding and evolution in patients who were immunocompromised during the omicron period: a multicentre, prospective analysis. Journal: Lancet Microbe.

Predicting progression of Alzheimer’s: New Tool

noreply@blogger.com (Unknown) — Sun, 28 Jan 2024 15:39:00 +0000

Approximately 55 million people worldwide are grappling with dementia, as reported by the World Health Organization, with Alzheimer's disease being the most prevalent form—a degenerative condition without a cure that leads to a decline in brain function.

Beyond the physical toll, Alzheimer's inflicts psychological, social, and economic consequences on both those living with the disease and their caregivers. Given the progressive nature of its symptoms, proactive planning for increased support becomes crucial as the disease advances.

Addressing this need, researchers at The University of Texas at Arlington have developed an innovative learning-based framework. This framework assists Alzheimer's patients in accurately identifying their position on the disease-development spectrum, facilitating better anticipation of the timing of later stages and aiding in planning for future care.

DAJIANG ZHU, AN ASSOCIATE PROFESSOR IN COMPUTER SCIENCE AND ENGINEERING AT UTA

Zhu, an associate professor in computer science and engineering at UTA, highlighted the continuous nature of Alzheimer's development and the transitional stages often overlooked by previous predictive approaches. Supported by over $2 million in grants from the National Institutes of Health and the National Institute on Aging, Zhu's team devised a learning-based embedding framework known as a "disease-embedding tree" (DETree). The DETree not only efficiently and accurately predicts the five fine-grained clinical groups of Alzheimer's development but also offers detailed status information, projecting the patient's position within it as the disease progresses.

Testing their DETree framework involved analyzing data from 266 individuals with Alzheimer's disease from the Alzheimer's Disease Neuroimaging Initiative. The DETree strategy outperformed other widely used methods for predicting Alzheimer's progression in multiple experiments, validating its efficacy using machine learning methods.

Zhu expressed optimism about the framework's accuracy, particularly in accommodating the varying rates at which individuals with Alzheimer's experience worsening symptoms. The team believes that the DETree framework holds promise beyond Alzheimer's and could potentially aid in predicting the progression of other diseases with multiple clinical stages, such as Parkinson's disease, Huntington's disease, and Creutzfeldt-Jakob disease.

JOURNAL: Pharmacological Research

Butterfly effect and autism spectrum disorder

noreply@blogger.com (Unknown) — Sun, 28 Jan 2024 15:33:00 +0000

A study conducted by researchers at the RIKEN Center for Brain Science (CBS) has shed light on the genetics of Autism Spectrum Disorder (ASD). They found that a particular type of genetic mutation contributes to ASD differently than typical mutations. By analyzing mutations in the genomes of individuals and their families, the researchers discovered that the three-dimensional structure of the genome can cause mutations to affect neighboring genes associated with ASD, even without mutations in ASD-related genes. The study was published in the scientific journal Cell Genomics on January 26.

ASD is a group of conditions characterized by repetitive behaviors and social interaction difficulties. Although the condition runs in families, its heritability is complex and only partially understood. According to studies, the high heritability cannot be explained by merely looking at the part of the genome responsible for protein coding. Instead, the answer could lie in the non-coding regions of the genome, particularly in promoters, which control whether proteins are produced. The team led by Atsushi Takata at RIKEN CBS examined "de novo" gene variants, which are new mutations not inherited from one's parents, in these parts of the genome.

Researchers analyzed large ASD whole genome sequencing data and found that promoter de novo mutations in TADs containing ASD genes were specifically associated with the disease.

The researchers analyzed a large dataset of over 5,000 families, making it one of the world's most extensive genome-wide studies of ASD to date. They focused on TADs, which are three-dimensional structures in the genome that enable interactions between nearby genes and their regulatory elements. They found that de novo mutations in promoters increased the risk of ASD only when the promoters were in TADs containing ASD-related genes. Because these mutations are nearby and in the same TAD, they can affect the expression of ASD-related genes. Therefore, the new study explains why mutations can increase the risk of ASD, even when they aren't in protein-coding regions or in the promotors that directly control ASD-related genes' expression.

"Our most important discovery was that de novo mutations in promoter regions of TADs containing known ASD genes are associated with ASD risk, and this is likely mediated through interactions in the three-dimensional structure of the genome," says Takata.

The researchers edited the DNA of stem cells using the CRISPR/Cas9 system to confirm their findings. They made mutations in specific promoters and found that a single genetic change in a promoter caused alterations in an ASD-associated gene within the same TAD. Takata compares the process to a genomic "butterfly effect" where a single mutation affects disease-associated genes scattered in distant regions of the genome.

Takata believes that this finding has implications for developing new diagnostic and therapeutic strategies. "When assessing an individual's risk for ASD, we now know that we need to look beyond ASD-related genes when doing a genetic risk assessment and focus on whole TADs containing ASD-related genes," explains Takata. "An intervention that corrects aberrant promoter-enhancer interactions caused by a promoter mutation may also have therapeutic effects on ASD."

Further research involving more families and patients is crucial to better understand the genetic roots of ASD. "By expanding our research, we will gain a better understanding of the genetic architecture and biology of ASD, leading to clinical management that enhances the well-being of affected individuals, their families, and society," says Takata.

JOURNAL Cell Genomics ARTICLE PUBLICATION DATE 26-Jan-2024

Insights into homologous recombination (DNA Repair) promise new insights into cancer

noreply@blogger.com (Unknown) — Sun, 21 Jan 2024 15:55:00 +0000

Researchers from Tokyo Metropolitan University have been studying DNA repair by homologous recombination, where the RecA protein repairs breaks in double-stranded DNA by incorporating a dangling single-strand end into intact double strands, and repairing the break based on the undamaged sequence. They discovered that RecA finds where to put the single strand into the double helix without unwinding it by even a single turn. Their findings promise new directions in cancer research.

Homologous recombination (HR) is a ubiquitous biochemical process shared across all living things, including animals, plants, fungi, and bacteria. As we go about our daily lives, our DNA is subjected to all kinds of environmental and internal stress, some of which can lead to breakage of both strands in the double helix. This can be disastrous, and lead to imminent cell death. Luckily, processes like HR are continuously repairing this damage.

Two competing models exist for homologous recombination. The results of this study support a model where the double-stranded DNA is not unwound during the homology search. (Shibata et al. Nucleic acids research, in press, DOI: 10.1093/nar/gkad1260, with modification)

During HR, one of the two exposed ends of the break in the helix falls away, revealing an exposed single-stranded end; this is known as resection. Then, a protein known as RecA (or some equivalent) binds to the exposed single strand and an intact double strand nearby. Next, the protein “searches” for the same sequence. When it finds the right place, it recombines the single strand into the double helix in a process known as strand invasion. The broken DNA strand is subsequently repaired using the existing DNA as a template. HR enables accurate repair of double-strand breaks, as well as the exchange of genetic information, making it a key part of biodiversity. But the exact biochemical picture of HR, including what happens when RecA carries both the single and double strands, is not yet clear.

A team led by Professor Kouji Hirota of Tokyo Metropolitan University has been studying DNA repair mechanisms like HR. In their most recent work, they sought to test two competing models for what happens when HR occurs. In one, RecA unwinds a section of the double strand during the “homology search,” where it tries to find the right place for strand invasion to occur. In the second, there is no unwinding after the binding of RecA; only when strand invasion takes place does any unwinding occur.

The team, in cooperation with a team from the Tokyo Metropolitan Institute of Medical Science, adopted two approaches to tackle which of these actually happens. In the first, they used a mutant of RecA which cannot separate the double strands i.e. cannot unwind the strand, to see whether this affected DNA repair. It turns out that this has minimal effect. In the second, they tried to measure how much torsion was created in the strand at different stages of the process. They found that the only torsion due to unwinding they could detect occurred after the homology search was complete i.e. when strand invasion occurred. For the first time, the team clearly showed that the second model was correct.

Detailed insights into homologous recombination are vital to understanding what happens when things go wrong. For example, factors implicated in breast cancer (BRCA1 and BRCA2) are also responsible for the correct loading of single-stranded DNA onto RAD51, the human version of RecA. This suggests that problems with HR might underlie high incidences of breast cancer in patients with hereditary defects in BRCA1 or BRCA2. The team hopes findings like theirs will lead to new directions for research into cancer.

This work was supported by JSPS KAKENHI Grant Number JP22K06335.

JOURNAL Nucleic Acids Research

DOI 10.1093/nar/gkad1260

12-Jan-2024

Cancer treatment through generative AI

noreply@blogger.com (Unknown) — Sun, 21 Jan 2024 04:20:00 +0000

Insilico Medicine(“Insilico”), a clinical stage generative artificial intelligence (AI)-driven drug discovery company, recently published an early research that it has identified MYT1 as a promising new therapeutic target for breast and gynecological cancer, and discovered a series of novel, potent, and highly selective inhibitors specifically targeting MYT1. These findings were supported by Insilico’s AI-driven generative biology and chemistry engine and published in the Journal of Medicinal Chemistry in Dec 2023.

Across the world, breast and gynecological cancers pose serious threats to women’s health, fertility, and overall quality of life. In order to identify potential targets for new therapeutics, the research team leverage Insilico's proprietary AI-driven target identification platform, PandaOmics, to analyze data of five forms of gynecological cancers, including ovarian, endometrial, cervical, and breast cancer particularly triple-negative breast cancer. Remarkably, MYT1 consistently ranked at the forefront across all diseases in terms of relevance.

MYT1 is a member of the Wee1-kinase family, rarely expressed in most normal tissues but highly expressed in most cancer types. It has been reported that MYT1 inhibition and CCNE1 amplification, a condition known as synthetic lethality, play crucial functions in cell cycle regulation, which indicates MYT1 inhibition is a promising synthetic lethal therapeutic strategy for the treatment of cancers with genome instability (e.g. CCNE1 amplification).

However, MYT1 is highly homologous to Wee1, which makes it challenging to design selective MYT1 inhibitors. In this study, Insilico addressed the gap in selective MYT1 inhibitors with the support of Chemsitry42, Insilico’s AI-driven small molecule generation platform. Using structure-based drug design (SBDD) strategies and applying rigorous filters for similarity and selectivity, Insilico designed an array of compounds targeting MYT1 from scratch. Amongst these novel compounds, one series emerged as hit compounds.

Insilico then conducted x-ray crystal structure analysis of the complex and found significant impact on the activity of subtle chemical structure modifications. This knowledge provided guidance for further molecular optimization, leading Insilico to the discovery of the lead compound, Compound 21. Compound 21 presents good MYT1 activity and excellent selectivity over Wee1 and the other kinase panel that reduces the potential risk for off-target effects and might translate to a safer profile. In preclinical studies, it also shows potent in vivo antitumor efficacy, and a promising profile in ADME and PK/PD.

“The innovative approach of this program has not only present a method for effective target identification but has also led to the development of a promising selective MYT1 inhibitor. ”said Yazhou Wang, Ph.D., medicinal chemistry leader of the MYT1 program from Insilico Medicine, and the first author of this paper. “Compound 21 expands Insilico's synthetic lethal pipeline and paves the way toward a safer, more effective therapeutic future for patients battling” gynecological and breast cancers.”

About Insilico Medicine

Insilico Medicine, a global clinical stage biotechnology company powered by generative AI, is connecting biology, chemistry, and clinical trials analysis using next-generation AI systems. The company has developed AI platforms that utilize deep generative models, reinforcement learning, transformers, and other modern machine learning techniques for novel target discovery and the generation of novel molecular structures with desired properties. Insilico Medicine is developing breakthrough solutions to discover and develop innovative drugs for cancer, fibrosis, immunity, central nervous system diseases, infectious diseases, autoimmune diseases, and aging-related diseases. www.insilico.com

JOURNAL: Journal of Medicinal Chemistry

DOI 10.1021/acs.jmedchem.3c01476

ARTICLE TITLE

Discovery of Tetrahydropyrazolopyrazine Derivatives as Potent and Selective MYT1 Inhibitors for the Treatment of Cancer

Role of metabolism-regulating signaling molecule (FAM3c) in breast cancer progression

noreply@blogger.com (Unknown) — Sat, 20 Jan 2024 20:44:00 +0000

A ground-breaking study conducted by Professor Jeong Park and his research team in the Department of Biological Sciences at UNIST has identified FAM3C, a metabolism-regulating signaling molecule produced by cancer-associated adipocytes (CAAs), that is involved in the development of breast cancer. As the main regulator of progress. Tumor microenvironment (TME). The findings, published in the prestigious academic journal Cancer Research, highlight the potential of targeted therapies in the treatment of breast cancer.

Study shows that overexpression of FAM3C in cultured adipocytes significantly reduces cell death in both adipocytes and co-cultured breast cancer cells while suppressing markers of fibrosis. In contrast, FAM3C deficiency in CAAs leads to adipocyte-mesenchymal transition (AMT) and increased fibrosis within the TME. The research team also discovered that breast cancer cells stimulate FAM3C expression in adipocytes through TGF-beta signaling, which can be blocked by a TGF-beta-neutralizing antibody.

In a genetically engineered mouse model of breast cancer, early depletion of FAM3C in CAs significantly inhibited primary and metastatic tumor growth. Furthermore, elevated levels of circulating FAM3C were observed in patients with metastatic breast cancer compared to patients with non-metastatic breast cancer.

Professor Jeong Park said, "These findings suggest that therapeutic inhibition of FAM3C expression in CAAs during early tumor development may hold promise as a novel approach in the treatment of breast cancer patients." "Understanding the role of cancer-associated adipocytes and their secreted molecules, such as FAM3C, opens new avenues for the development of early diagnostic markers and targeted therapies for breast cancer."

The findings of this study have been published in the online edition of Cancer Research on December 20, 2023. The research was conducted in collaboration with the National Research Foundation of Korea (NRF), funded by the Ministry of Science and ICT (MSIT). , Basic Science Research Program, as well as a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health and Welfare of the Republic of Korea.

Reference:

Sahi Kim, Jeong Oh, Chanho Park, et al., "FAM3C in cancer-associated adipocytes promotes survival and metastasis of breast cancer cells," Cancer Research, (2023).

Unraveling the Mysteries: Exploring New Genetic Variants Related to Dementia

noreply@blogger.com (Unknown) — Tue, 16 Jan 2024 04:00:00 +0000

Introduction:

Dementia, a debilitating condition affecting millions worldwide, has long been a subject of intense research. Scientists and researchers have tirelessly worked towards understanding its underlying causes, and recent breakthroughs in genetics have brought forth new hope. This blog post delves into the latest discoveries surrounding genetic variants linked to dementia, shedding light on the potential implications for both diagnosis and treatment.

The Human Genome Project and Beyond:

Advancements in genetic research, particularly since the completion of the Human Genome Project, have paved the way for a deeper understanding of the intricate relationship between genes and various health conditions, including dementia. The identification of specific genetic variants associated with an increased risk of developing dementia has become a pivotal focus.

Key Genetic Variants:

Recent studies have unveiled several genetic variants implicated in the onset and progression of dementia. One such variant is APOE ε4, a gene associated with an elevated risk of Alzheimer's disease, the most common form of dementia. However, new research is expanding the scope beyond APOE ε4, revealing additional genetic markers that contribute to the complexity of dementia-related disorders.

Polygenic Risk Scores:

The concept of polygenic risk scores has gained prominence in the realm of dementia research. Scientists are exploring the combined impact of multiple genetic variants to create risk scores that can predict an individual's susceptibility to dementia. This approach allows for a more comprehensive assessment, considering the intricate interplay of various genes in influencing cognitive health.

Genetic Insights into Different Dementia Types:

Dementia is not a singular entity but rather a diverse spectrum of disorders. Researchers are now making strides in understanding the genetic underpinnings of different types of dementia, such as vascular dementia, frontotemporal dementia, and Lewy body dementia. Unraveling the genetic intricacies of each type opens avenues for targeted therapies tailored to specific forms of the condition.

Implications for Diagnosis and Treatment:

The identification of new genetic variants related to dementia holds immense promise for early diagnosis and personalized treatment strategies. Genetic testing may become a valuable tool in assessing an individual's risk and providing insights into potential preventive measures. Moreover, understanding the genetic basis of dementia may pave the way for the development of innovative therapeutic interventions targeting specific genetic pathways.

Ethical Considerations:

While the potential benefits of genetic research in dementia are vast, ethical considerations must be at the forefront. Privacy concerns, the potential for genetic discrimination, and the need for informed consent underscore the importance of responsible and transparent genetic testing practices.

Conclusion:

The exploration of new genetic variants related to dementia marks a significant leap forward in our quest to comprehend and combat this challenging condition. As research continues to unravel the intricate genetic tapestry of dementia, the prospect of early diagnosis, targeted treatments, and personalized care becomes increasingly tangible. The journey to unlock the secrets of dementia is ongoing, but each breakthrough brings us one step closer to a future where the impact of this condition is significantly mitigated.

Understanding the Complex Interplay: Dementia and Genetic Changes

noreply@blogger.com (Unknown) — Tue, 16 Jan 2024 03:56:00 +0000

Introduction:

Dementia is a challenging and multifaceted condition that affects millions of individuals worldwide. As our understanding of the factors contributing to dementia expands, one crucial aspect gaining attention is the role of genetic changes. This blog post aims to explore the intricate relationship between dementia and genetic factors, shedding light on the complexities of this neurological disorder.

I. The Genetic Landscape of Dementia:

Dementia encompasses a range of cognitive disorders, with Alzheimer's disease being the most prevalent form. While environmental factors and lifestyle choices play a role in dementia development, genetic changes are increasingly recognized as significant contributors.

A. Familial Patterns:

Research has identified certain familial patterns in dementia, indicating a genetic predisposition for some individuals. Families with a history of dementia may carry specific gene variants that increase the risk of developing the condition. Understanding these genetic links is crucial for early detection and intervention.

B. Genetic Variants and Risk Factors:

Several genes have been implicated in dementia risk. The APOE gene, for example, is associated with an increased likelihood of developing Alzheimer's disease. Exploring these genetic variants helps researchers unravel the biological mechanisms behind dementia and develop targeted treatments.

II. The Complex Genetics of Alzheimer's Disease:

Alzheimer's disease, the most common form of dementia, involves intricate genetic changes that impact brain function and structure.

A. Beta-Amyloid and Tau Proteins:

Genetic mutations can lead to the abnormal accumulation of beta-amyloid and tau proteins in the brain, hallmark characteristics of Alzheimer's. Understanding how these proteins interact and disrupt neural function is vital in deciphering the genetic basis of the disease.

B. Early-Onset Alzheimer's and Genetic Mutations:

In some cases, Alzheimer's disease manifests earlier in life due to specific genetic mutations. Unraveling the genetic basis of early-onset Alzheimer's can provide insights into potential preventive measures and targeted therapies.

III. Genetics, Lifestyle, and Dementia Risk Reduction:

While genetics play a role in dementia, it is essential to recognize the interplay between genetic factors and lifestyle choices.

A. Modifiable Risk Factors:

Certain lifestyle modifications, such as maintaining a healthy diet, regular exercise, and cognitive stimulation, can mitigate dementia risk, even in individuals with a genetic predisposition.

B. Personalized Approaches:

Understanding an individual's genetic risk profile allows for personalized interventions. Genetic testing may enable targeted strategies for lifestyle modifications, early detection, and personalized treatment plans.

Conclusion:

Dementia and genetic changes are intertwined in a complex dance, with each influencing the other. While genetic factors contribute to susceptibility, lifestyle choices and environmental factors play a pivotal role in shaping an individual's dementia risk. Advances in genetic research offer hope for early detection, personalized interventions, and innovative treatments, bringing us closer to a future where we can better understand and manage this challenging condition.

Navigating the Landscape of Dementia: Unveiling the Current Risk Factors in 2024

noreply@blogger.com (Unknown) — Sun, 14 Jan 2024 17:17:00 +0000

Dementia, a condition characterized by a decline in cognitive abilities affecting daily life, has become a growing concern worldwide. As we step into 2024, it's crucial to explore the latest insights into dementia and its associated risk factors. Understanding these factors is essential for early detection, prevention, and providing better care for those affected.

Age:

Age remains one of the primary risk factors for dementia. As individuals grow older, the likelihood of developing dementia increases. While it's not an inevitable consequence of aging, the risk does rise significantly after the age of 65. Researchers continue to study the complex interplay of genetic and environmental factors contributing to age-related cognitive decline.

Genetics:

Genetic factors play a pivotal role in dementia risk. Advances in genomic research have identified certain genes associated with an increased susceptibility to dementia. Familial history can be a crucial indicator, with some individuals having a higher genetic predisposition to conditions like Alzheimer's disease. Genetic testing is becoming more sophisticated, providing insights into an individual's risk profile.

Lifestyle and Cardiovascular Health:

Recent research highlights the connection between lifestyle choices and dementia risk. Adopting a heart-healthy lifestyle, including regular exercise, a balanced diet, and maintaining cardiovascular health, has been linked to a lower risk of developing dementia. Managing conditions like hypertension, diabetes, and high cholesterol can contribute to overall brain health.

Cognitive Engagement:

Keeping the brain active through cognitive engagement has emerged as a protective factor against dementia. Activities such as learning new skills, engaging in mentally stimulating hobbies, and maintaining social connections contribute to cognitive reserve—a buffer that may delay the onset of dementia symptoms.

Environmental Factors:

Environmental factors, including exposure to certain toxins and pollutants, are being investigated for their potential role in dementia risk. Studies are ongoing to understand how air quality, environmental toxins, and other external factors may contribute to cognitive decline.

Traumatic Brain Injury (TBI):

A history of traumatic brain injury, particularly repeated injuries, has been identified as a potential risk factor for dementia. Athletes in contact sports and individuals with a history of accidents leading to head injuries are being studied to better understand the long-term consequences of TBIs on cognitive function.

Mental Health:

Mental health conditions, such as depression and anxiety, have been linked to an increased risk of dementia. Addressing mental health issues and seeking appropriate treatment may contribute to a lower risk of cognitive decline.

Conclusion:

As we delve into 2024, our understanding of dementia and its risk factors continues to evolve. Age, genetics, lifestyle choices, environmental factors, traumatic brain injuries, and mental health all play integral roles in shaping an individual's risk profile. Ongoing research promises to unravel more insights, paving the way for improved preventive strategies and enhanced care for those affected by dementia. It is a collective effort to raise awareness, support research, and foster a society that values brain health as an integral part of overall well-being.

May be not Alzheimer's but hearing loss related memory problems

noreply@blogger.com (Unknown) — Mon, 21 Jan 2019 05:18:00 +0000

Older adults concerned about displaying early symptoms of Alzheimer's disease should also consider a hearing check-up, suggest recent findings.

What might appear to be signs of memory loss could actually point to hearing issues, says Dr. Susan Vandermorris, one of the study's authors and a clinical neuropsychologist at Baycrest.

A recent Baycrest study, published in the Canadian Journal on Aging, found that the majority (56 per cent) of participants being evaluated for memory and thinking concerns and potential brain disorders had some form of mild to severe hearing loss, but only about 20 per cent of individuals used hearing aids. Among the participants, a quarter of them did not show any signs of memory loss due to a brain disorder.

"We commonly see clients who are worried about Alzheimer's disease because their partner complains that they don't seem to pay attention, they don't seem to listen or they don't remember what is said to them," says Dr. Vandermorris. "Sometimes addressing hearing loss may mitigate or fix what looks like a memory issue. An individual isn't going to remember something said to them if they didn't hear it properly."

Hearing loss is the third most common chronic health condition in older adults, which is experienced by 50 per cent of individuals over the age of 65 and 90 per cent of people over the age of 80. It takes an average of 10 years before people seek treatment and less than 25 per cent of individuals who need hearing aids will buy them.

Hearing status is not always addressed in neuropsychology clinics, but can impact performance on memory assessments done verbally, adds Dr. Vandermorris.

"Some people may be reluctant to address hearing loss, but they need to be aware that hearing health is brain health and help is available," she adds.

The study analyzed results from 20 individuals who were receiving a neuropsychological assessment at Baycrest. Participants completed a hearing screening test after their cognitive evaluation.

Neuropsychologists were privy to hearing test results after their initial assessment, which altered some of their recommendations. For example, some clients were referred to a hearing clinic for a full audiology assessment or to consider using a hearing aid, as well as provided education on hearing loss and communication.

"Since hearing loss has been identified as a leading, potentially modifiable risk factor for dementia, treating it may be one way people can reduce the risk," says Marilyn Reed, another author on the study and practice advisor with Baycrest's audiology department. "People who can't hear well have difficulty communicating and tend to withdraw from social activities as a way of coping. This can lead to isolation and loneliness, which can impact cognitive, physical and mental health."

This study builds on earlier research that analyzed how addressing memory problems could benefit older adults seeking hearing loss treatment.

"We are starting to learn more about the important role hearing plays in the brain health of our aging population," says Dr. Kate Dupuis, lead author on the study, a former postdoctoral fellow at Baycrest, clinical neuropsychologist and Schlegel Innovation Leader at the Sheridan Centre for Elder Research. "In order to provide the best care to our older clients, it is imperative that neuropsychologists and hearing care professionals work together to address the common occurrence of both cognitive and hearing loss in individuals."

Since the studies, Baycrest's Neuropsychology and Cognitive Health Program and Hearing Services have incorporated general screening for hearing and memory issues into their assessments, as well as provided educational materials to clients.

Next steps for the study will involve optimizing screening strategies for hearing loss in memory assessments and ongoing interprofessional collaborations to create educational tools that counsel clients about the relationship between hearing, memory and brain health.

###

The study was made possible with support from the neuropsychology and cognitive health and audiology programs at Baycrest. The research team included Iris Yusupov, Dr. Kelly Murphy, Dr. Dmytro Rewilak and Dr. Kathryn Stokes.

SOURCE: BAYCREST CENTRE FOR GERIATRIC CARE

Long Sleeping hours during pregnancy and late stillbirth may be linked

noreply@blogger.com (Unknown) — Mon, 21 Jan 2019 05:16:00 +0000

Sleeping more than nine hours per night during pregnancy may be associated with late stillbirth, a new Michigan Medicine-led international study suggests.

Researchers analyzed online surveys involving 153 women who had experienced a late stillbirth (on or after 28 weeks of pregnancy) within the previous month and 480 women with an ongoing third-trimester pregnancy or who had recently delivered a live born baby during the same period.

The findings, which appear in journal Birth, suggest an association between lengthy periods of undisturbed maternal sleep and stillbirths that were independent of other risk factors. But researchers caution that further research is needed to better understand the relationship and what it means for pregnant women.

"Pregnant women often report waking up and getting up in the middle of the night," says lead author Louise O'Brien, Ph.D., M.S., a University of Michigan researcher in the Division of Sleep Medicine, Department of Neurology and the Department of Obstetrics and Gynecology at Michigan Medicine.

"While multiple awakenings during the night may concern some women, in the context of stillbirth it appears to be protective."

O'Brien says further studies need to delve deeper into what may drive the relationship between maternal sleep and stillbirths, with particular focus on how the autonomic nervous system - the control system that regulates bodily function - and the hormonal system are regulated during sleep in late pregnancy.

She notes that blood pressure reaches its lowest point during sleep but when someone is awakened, there is a surge in the nervous system activity that causes transient increases in blood pressure. It's possible that these brief increases in blood pressure are able to prevent long periods of relatively low pressure. This is important, O'Brien says, because low blood pressure has been linked with fetal growth problems, preterm birth, and stillbirth.

O'Brien also cautions that "pregnant women should not be waking themselves up at night." Very disruptive sleep has also been associated with poor pregnancy outcomes, including growth restriction and preterm growth.

She notes that while there is already evidence that very disrupted sleep and clinical sleep disorders are associated with poor pregnancy outcomes, few studies have looked at the opposite end of the spectrum, such as long periods of undisturbed sleep

"Our findings add to research indicating that maternal sleep plays a role in fetal wellbeing," she says. "Studies aiming to reduce stillbirths should consider maternal sleep as this is a potentially modifiable risk factor. Understanding the role of maternal sleep may help us identify interventions that would put us in a better position to advise women."

Stillbirth effects about 1 in 160 pregnancies in the U.S., with about 24,000 babies stillborn in the country every year - 10 times as many deaths that occur from Sudden Infant Death Syndrome (SIDS). About half of all stillbirths happen after 28 weeks of pregnancy and many remain unexplained.

Rates are even worse in low income countries but the stillbirth rate in the U.S. is still higher than in many other Western countries

Smoking, advanced maternal age, diabetes, obesity and drug abuse are among well-established risk factors for stillbirths. Maternal sleep practices, however, cover a relatively new area of investigation.

The new study follows other research looking at possible ties between maternal sleep and fetal wellbeing in recent years, including studies suggesting that women who report that they sleep on their backs have an increased risk of stillbirths. While the current study asked about maternal sleep position, not enough women reported sleeping on their backs for any meaningful analysis.

"Maternal sleep has been overlooked as a potential area for maternal and newborn health interventions even though it is related to many of the major, well-established risk factors for poor pregnancy outcomes. Until recently, it hasn't been on the radar for stillbirth research," O'Brien says.

"Many risk factors for stillbirths are not able to be modified once pregnancy has begun. But we should be looking at every possible intervention that may prevent poor outcomes. Progress in reducing stillbirth deaths has been slow but stillbirth is an urgent global health issue that should be at the center of more research programs."

SOURCE: MICHIGAN MEDICINE - UNIVERSITY OF MICHIGAN

Natural Solution to Skin Wrinkles Comes From Maple Leaf Extract

noreply@blogger.com (Unknown) — Tue, 21 Aug 2018 12:18:00 +0000

Maple trees are best known for their maple syrup and lovely fall foliage. But it turns out that the beauty of those leaves could be skin-deep -- and that's a good thing. Today, scientists report that an extract from the leaves may prevent wrinkles.

The researchers are presenting their results at the 256th National Meeting & Exposition of the American Chemical Society (ACS). ACS, the world's largest scientific society, is holding the meeting here through Thursday. It features more than 10,000 presentations on a wide range of science topics.

The scientists had previously studied the chemistry and health benefits of sap and syrup obtained from sugar maple and red maple trees. Historical records suggested that other parts of the trees could also be useful, according to Navindra P. Seeram, Ph.D., the project's principal investigator. "Native Americans used leaves from red maple trees in their traditional system of medicine," he notes, "so why should we ignore the leaves?"

Skin elasticity is maintained by proteins such as elastin. Wrinkles form when the enzyme elastase breaks down elastin in the skin as part of the aging process. "We wanted to see whether leaf extracts from red maple trees could block the activity of elastase," says Hang Ma, Ph.D., who is presenting the work at the meeting and is a research associate in Seeram's lab.

The researchers, who are at the University of Rhode Island, zeroed in on phenolic compounds in the leaves known as glucitol-core-containing gallotannins (GCGs) and examined each compound's ability to inhibit elastase activity in a test tube. The scientists also conducted computational studies to examine how the GCGs interact with elastase to block its activity, and how the molecules' structures affect that blocking ability. GCGs containing multiple galloyl groups (a type of phenolic group) were more effective than those with a single galloyl group. But these compounds can do more than interfere with elastase. In prior work, Seeram's group showed that these same GCGs might be able to protect skin from inflammation and lighten dark spots, such as unwanted freckles or age spots.

Seeram and Ma plan to do further testing. "You could imagine that these extracts might tighten up human skin like a plant-based Botox®, though they would be a topical application, not an injected toxin," Seeram says. And the fact that the extracts are derived from trees would be appreciated by consumers who are looking for natural, plant-based ingredients in their skincare products.

The researchers have taken steps to get the extracts into products, having developed a proprietary patent-pending formulation containing GCGs from summer and fall maple leaves and maple sap, which they named MaplifaTM (pronounced "mape-LEAF-uh" to reflect its origin). They have licensed it to botanical extracts supplier Verdure Sciences based in Indiana and are hoping to eventually find a market for the formulation in the cosmetics sector or even in dietary supplements.

If these products come to fruition, the team's findings could benefit the local economy. "Many botanical ingredients traditionally come from China, India and the Mediterranean, but the sugar maple and the red maple only grow in eastern North America," Seeram says. Farmers in the region, who currently only harvest sap from the maple trees, could tap the leaves as a value-added product for an additional source of income. Even better, the process would be sustainable because leaves could be collected during normal pruning or when they fall from the trees in autumn.

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Skin cell research
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Health and subcutaneous fat
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Original Abstract:

Skin wrinkling is a declining process of skin cell function associated with aging caused by the loss of skin elasticity over time. Skin elasticity is maintained by skin extracellular matrix proteins such as elastin. Elastase, a member of the chymotrypsin family of proteases, is responsible for the breakdown of skin elastin. Therefore, inhibition of elastase enzyme is a plausible management for skin elastin degradation and thus, elastase inhibitors, including natural products, are being investigated as anti-wrinkle cosmetic agents. We previously reported on the skin protective effects, including anti-glycation and anti-melanogenic properties, of a series of glucitol-core containing gallotannins (GCGs) from a proprietary phenolic-enriched red maple (Acer rubrum) leaves extract (MaplifaTM). However, the effect of these GCGs on elastase enzyme is unknown. Herein, we investigated the inhibitory effects of MaplifaTM GCGs including ginnalin B (GB), ginnalin C (GC), ginnalin A (GA), maplexin F (MF) and maplexin J (MJ) on elastase enzyme. The GCGs (at 500 μM) showed inhibitory activities ranging from 21.3 - 62.5% and the GCGs with multiple galloyl group including GA (2 galloyls), MF (3 galloyls), and MJ (4 galloyls) showed superior activity to those GCGs with a mono-galloyl group (namely, GB and GC). The mechanisms of the GCGs' inhibitory effects on elastase enzyme were further studied by using an enzyme kinetic assay and computational docking method. Our data suggest that MaplifaTM GCGs may have anti-wrinkle activity through the inhibition of elastase enzyme warranting further studies on its cosmetic applications.

Source: American Chemical Society