Research Blogging - Neuroscience - English

Neuroscientists should study Zombie Ants

2012-05-25T15:32:00Z

Zombie ant controlled by fungus (source)The fungus-controlled zombie ant is one of natures' greatest wonders. A fungus (e.g. O. Unilateralis) is inhaled by an ant (e.g. Camponotus Leonardi), and begins to grow inside its body. Eventually the fungus infests the brain of the ant, causing it to drunkenly wander, periodically convulse, climb up a leaf and clamp down on its ridge. Once the ant is securely in place, the fungus devours the brain and innards of the ant and grows out the back of its head often (but not always) releasing its spores onto the ground below. Un-freaking-believable, right?As if this wasn't amazing enough, it's not like it is only one fungus species that infects only one ant species. There are many of these fungi and they infect many different kinds of insect, but somehow maintain a species specificity. In other words, fungus#1 can infect SpeciesX, but not SpeciesY, and Fungus#2 infects SpeciesY, but not SpeciesQ, and so forth. So WHY does this happen? and HOW has no one looked at the brain cells of these ants? Though no one has looked at the brains of these ants, Last year a paper painstakingly characterized their behavior under 'fungi control'. The most interesting characteristics are:The ants display a 'drunkard's walk' (the author's words)The ants periodically spasm and fall down (if they are above ground level)The ants clamp down on the underside main vein of a leaf (never the side of the leaf, never the top) Interestingly they all bite down on the leaf around solar noon.Figure 1, Hughes et al., 2011This figure shows the behavior of several ants. Each ant was observed during the time of the horizontal blue bar. The black vertical lines and 'spasms' which caused the ants to fall down (gray stars), and the red triangles are when the ant bit down on the leaf ridge. Because we have no idea how the fungus is manipulating the ant, let's wildly speculate.1. The Drunken Walk:Why: The reason for this is not clear. The ant doesn't go far, so the non-directional walking could be to keep it close to more ants.How: The mechanism is also not clear, but usually an ants directional walking could be following a pheromone trail. The fungus could presumably cause random walking by confusing the ants ability to sense pheromones. It could possibly even cause 'hallucinatory' pheromone sensing.2. The Periodic Spasms: Why: The authors speculate that the purpose of these spasms is to keep the ant near the ground. The infect ants spend much more time on the ground level than the uninfected ants, and the spasms are often followed by a fall.How:A fungus could essentially cause a seizure in the ants brain by manipulating potassium or calcium channels. On the other hand, I suppose the fungus could be acting directly on the muscles, causing them to twitch in an uncontrolled way. 3. The Clamping: Why: This has an obvious function, to root the ant for ultimate fungal growth and dispersion. How: First of all, biting and even walking on leaves is not something these ants normally do. So the fungus isn't just hijacking a behavior that the ant already has, it's basically creating a new one. The correlation with solar noon indicates that a light or heat signal could contribute to the trigger, but basically nothing else is known about it. Interestingly, the clamping does not always have to be one single event either. A few of the ants clamped down on the leaf vein more than once. The authors of this paper spend time discussing fungi's direct effect on the mandible muscles of the ant.Figure 3 Hughes et al., 2011They show that the mandible muscles of the normal ant are fat and healthy (B), but the muscles of the infected ant are separated and reduced in size (C). Though this image is of an ant at the moment of biting, the authors suggests that the deterioration of the mandible muscle might be to prevent re-opening of the clamp. They do not speculate on how the clamp is initiated in the first place, or why it occurs at noon. So please, fellow neuroscientists, somebody stain these brains! It's just too fascinating to resist exploration. What proteins are altered? What is the receptor composition of behaviorally-specific neurons? Are the dendrites differently shaped? And who knows what sort of great advances might be hidden in these brain-controlling fungi. The magic of optogenetics comes from lowly light-sensitive bacteria, just think of the possibilities hidden in brain-controlling fungus. To be fair, some neuroscience has been done on parasitic brain control, but it is very limited. In fact it is limited to basically one histological study about parasitic worms who infest crickets and cause them to drown themselves (the subject of a future blog post). However, suicide-crickets are no zombie-ants and the exact mechanisms of the interaction © TheCellularScaleHughes DP, Andersen SB, Hywel-Jones NL, Himaman W, Billen J, & Boomsma JJ (2011). Behavioral mechanisms and morphological symptoms of zombie ants dying from fungal infection. BMC ecology, 11 (1) PMID: 21554670...

Hughes DP, Andersen SB, Hywel-Jones NL, Himaman W, Billen J, & Boomsma JJ. (2011) Behavioral mechanisms and morphological symptoms of zombie ants dying from fungal infection. BMC ecology, 11(1), 13. PMID: 21554670

Brain Connectivity Alterations in OCD

2012-05-25T11:51:41Z

Obsessive compulsive disorder (OCD) is an anxiety disorder characterized by intrusive thoughts interfering with everyday activities. The prevalence of OCD is estimated to be between 1 to 2 percent of the population. Despite several approved drug treatments and the availability of behavioral therapy, many individuals with OCD find their symptoms resistant to treatment. A better understanding of the underlying pathophysiology of OCD is needed for the development of more effective treatment.A recent brain imaging study provides some additional insight into the connectivity alterations found in those with OCD. In this study, 30 subjects with OCD were compared to a group of 32 control subjects using functional magnetic resonance imaging. The subjects were studied for functional connectivity of the default mode network (DFM) as well as the fronto-parietal network (FPN).The default mode network is the working network of brain regions typically active "at rest" when no specific brain-related task is being performed. You might think of this as what brain regions are in synchronization with each other during rest. We know that individuals with OCD commonly find their resting brain state is disrupted by their intrusive obsessional thoughts. This makes study of the default mode network promising for understanding OCD.The key findings in OCD from this study were:Reduction in the typical negative correlation between the DFM and the FPNAltered connectivity between the anterior insula and multiple DFM regions including the parahippocampus, medial frontal cortex, posterior cingulate cortex, and the posterior inferior parietal lobeIncreased connectivity of the FPN with regions outside the DFM including the thalamus, lateral frontal cortex and somatosensory/motor brain regionsThe authors note "Though speculative, the current findings of attenuated negative connectivity between anterior insula and DMN suggest a potential neural basis for the difficulty OCD patients may have in efforts to disengage from internal mental processes in order to respond to more appropriately salient external information related to potential risk (such as that informing them that dreaded events have not or will not occur)."The authors also note their study may not represent findings specific to OCD but may be related to broader anxiety conditions. This will need to be explored by contrasting differences (and similarities) across OCD with other anxiety disorders such as generalized anxiety disorder, panic disorder, social anxiety disorder and PTSD.This study is indicative of the evolving conceptualization of many mental disorders. Many mental disorders appear to not be due to a single neurotransmitter abnormality or a localized brain lesion but appear to be abnormalities of brain circuitry. Functional brain connectivity imaging of the DMN holds promise as a tool to better understand these circuitry alterations.Photo of female adult black bear from Lake Istasca State Park from the author's files.Stern, E., Fitzgerald, K., Welsh, R., Abelson, J., & Taylor, S. (2012). Resting-State Functional Connectivity between Fronto-Parietal and Default Mode Networks in Obsessive-Compulsive Disorder PLoS ONE, 7 (5) DOI: 10.1371/journal.pone.0036356...

Stern, E., Fitzgerald, K., Welsh, R., Abelson, J., & Taylor, S. (2012) Resting-State Functional Connectivity between Fronto-Parietal and Default Mode Networks in Obsessive-Compulsive Disorder. PLoS ONE, 7(5). DOI: 10.1371/journal.pone.0036356

Hearing radio frequencies

2012-05-24T17:36:10Z

I was reading the Wikipedia article on tinnitus, and came across this pearl of a sentence: A common and often misdiagnosed condition that mimics tinnitus is Radio Frequency (RF) Hearing in which subjects have been tested and found to hear high-pitched transmission frequencies that sound similar to tinnitus. Hmm, what? Yes, humans, under special circumstances, [...]...

Elder, J., & Chou, C. (2003) Auditory response to pulsed radiofrequency energy. Bioelectromagnetics, 24(S6). DOI: 10.1002/bem.10163

The Anorexic Brain: A Summary of Neuroimaging Studies - Part 1

2012-05-23T20:16:00Z

One of the best ways to get an introduction to a particular field is by reading review articles. Review articles summarize the latest findings in the field, discuss the limitations and gaps in our present knowledge, and suggest future research directions. They also give a good overview of where the scientific consensus lies. Journalists prefer to report on novel and exciting findings regardless of how likely they are to be replicated or how well they fit in with everything else we know about that topic. It is an all too common occurrence that a small pilot study which has favourable results, creates a buzz in and gets into our heads, only to produce negative or unfavourable results once the sample size is increased. But this, of course, never makes it to the printing press. So we are left thinking the results of the pilot study are correct when they might be an outlier, or just a false positive....

Pietrini, F., Castellini, G., Ricca, V., Polito, C., Pupi, A., & Faravelli, C. (2011) Functional neuroimaging in anorexia nervosa: A clinical approach. European Psychiatry, 26(3), 176-182. DOI: 10.1016/j.eurpsy.2010.07.011

Video Tip of the Week: the New PubMed Filters Sidebar

2012-05-23T08:49:17Z

In today’s tip I am linking to a YouTube video from NCBI that briefly explains the new Filters Sidebar feature that has been added to PubMed. We first saw a tweet that the change was coming back on May 2nd, just as I was completing a total update to our full PubMed tutorial*. I struggled with [...]...

Sayers E. W., Barrett T., Benson D. A., Bolton E., Bryant S. H., Canese K., Chetvernin V., Church D. M., DiCuccio M., & Federhen S. (2011) Database resources of the National Center for Biotechnology Information. Nucleic Acids Research, 40(D1). DOI: 10.1093/nar/gkr1184

Neurons are like equations

2012-05-22T23:22:00Z

The brain of the clock (I took this picture)A computational model is a surrogate version of something usually made on a computer. An example that most people are familiar with are the computational models used to predict the weather. If you know how low pressure and high pressure fronts interact, and you know where one is and how fast it is moving, you can program software to play the situation out in a simulation, predicting what will happen and how quickly. Computational neuroscience is more or less just like that and it can be used to investigate all levels of neuroscience. Here's a brief intro to three of the basic levels. There are other types of computational models in neuroscience, but these three make up most of them.The Whole BrainIf you know how the thalamus, hippocampus, amygdala, and cortex all work together, you can simulate how inputs into one structure might influence the others. In this case each brain structure would basically be a 'black box' that received input and produced output based on known data. To do this kind of simulation you wouldn't actually simulate the millions of neurons in each structure.The Neural Network(source)On the next level down, you can make a computational model of a neural network inside a single brain structure. If you know the types of neurons in the amygdala and how they interact with each other, you can program those relationships in and test what might happen if one class of neurons fires too much or too little. You can test the effect removing one class of neurons has on the whole network and the output of that brain structure. In this case you are simulating individual neurons, but you are probably not simulating the details of the neurons, such as their dendrites and their specific channel composition. In this kind of computational model, the neurons are the 'black box' which receive input and produce output based on pre-set equations.The Cellular ScaleOne level down from this is a computational model of an individual neuron. In this type of model, the neuron is simulated in detail, with its dendrites, soma, and sometimes the axon. With this kind of model, you can test the effects of different dendrite shapes on the processing of the neuron. Usually the individual channels (such as calcium, potassium and sodium channels) in the neuron are programmed in and the electrical properties of the cells are calculated in detail. In this situation, the specific proteins and channels are the 'black boxes' computing ionic concentrations based on pre-set equations. A detailed tutorial on how to make a biophysically realistic model neuron can be found here.a neuron can be simulated as a series of resistors and capacitorsSidiropoulou et al., (2006) have an excellent review of the neuroscience discoveries that have been made with this cellular level of computational modeling. They start their paper highlighting the most interesting problem in cellular neuroscience."Understanding how the brain works remains one of the most exciting and intricate challenges of modern biology. Despite the wealth of information that has accumulated during the past years about the molecular and biophysical mechanisms that underlie neuronal activity, similar advances have yet to be made in understanding the rules that govern information processing and the relationship between the structure and function of a neuron." (Intro, Sidiropoulou et al., 2006) (red mine)This paper directly argues against the idea that neurons are just 'on-off' switches, and illustrates the complex computational processes that occur in individual locations of the neuron. They cover computational studies analyzing the information processing that occurs in the dendrite, at the synapse, at the soma, and even in the axon. The details are to complicated to get into here, but the paper is free. Finally, they end with a call to action for experimental and computational neuroscientists to work together to solve the really interesting problems in cellular neuroscience. "The following open questions could provide fertile ground for collaborations among molecular biologists, geneticists, physiologists, modellers and behaviourists for further explorations of the mysteries of the brain. Do specific behaviours require certain neuronal computational tasks? Which parts of the neural circuit or the neuron itself are responsible for these tasks? What are the underlying molecular mechanisms for the distinct operating modes of neuronal integration? Such holistic approaches should lend support to the growing idea reinforced by this review: that something smaller than the cell lies at the heart of neural computation." (Discussion, Sidiropoulou et al., 2006)Just as computational models can predict weather patterns with some degree of accuracy, no model is perfect. Similarly computational neuroscience is not going to lead to all the answers, but where it is particularly useful is in making very specific predictions about how certain aspects of a neuron or neural circuit might work. The insight gained from computational models can guide and focus experiments, making them more efficient. This saves time, money, energy, and animal lives. © TheCellularScaleSidiropoulou K, Pissadaki EK, & Poirazi P (2006). Inside the brain of a neuron. EMBO reports, 7 (9), 886-92 PMID: 16953202...

Sidiropoulou K, Pissadaki EK, & Poirazi P. (2006) Inside the brain of a neuron. EMBO reports, 7(9), 886-92. PMID: 16953202

The Wacky World of Evolutionary Psychology

2012-05-22T14:08:00Z

Evolution is surely my favourite of all scientific theories. Sure, stars dying so that we could live is astoundingly humbling, and the sheer incomprehensibility of quantum mechanics is what makes it so intellectually titillating, but evolution explains the origins and inter-connectedness of the universe’s most glorious feat: life. And yet, despite having developed these marvellous mammalian brains, we are fallible creatures prone to idiocy, and evolution is a theory widely abused. Some time ago, I posted briefly on the peculiar world of evolutionary psychology. While it is an area that holds much promise, it also lends undeserved credibility to biases and ill-conceived hypotheses. Dr. Satoshi Kanazawa, who labels himself the “Scientific Fundamentalist”, seems to be one of the most profligate producers of bad ideas that I’ve come across. Last year, he was investigated for claiming that research demonstrates black women are less attractive; more recently he dubiously suggested that gay people are smarter than average; and I just came across another claim that people who listen to classical music must be smarter too. As a gay classical music lover (sadly not black), these are very flattering assertions, but the logic underpinning them is shameful. It’s perhaps worth noting that Kanazawa’s profile page includes two quotations and a personal warning about offending people with the “truth”, so I wouldn’t be surprised if he occasionally feels the need to be controversial at the cost of reason. Both his claims about the intelligence of gay people and classical music fans rest on what he calls the Savanna-IQ Interaction Hypothesis, which theorises that traits and behaviours that are relatively novel in human evolutionary history are correlated with greater intelligence. In other words, if you like things that haven’t been around that long on an evolutionary time-scale, you can be proud of your IQ, but if you enjoy things that our species has enjoyed for millennia, you’re a bit of a moron. I don’t know if Kanazawa has any reasonable substantiation for the Savanna Hypothesis - I’m not sure I have the time or courage to subject myself to his writings - but I want to humour the idea and attempt to demonstrate that, even if true, same-sex- and classical-music-loving are not candidates for greater intelligence on such grounds. First, homosexuality. Bearing in mind that the most important facet of this idea is that the phenomenon must be evolutionarily novel, it ought to be obvious to someone even vaguely familiar with human sexual biology that homosexuality cannot be considered new. For starters, we know from the prevalence of homosexuality across cultures and time periods (many of which feature same-sex intercourse without the concepts of hetero-/bi-/homo- sexualities that exist today) that it is not necessary to have a hereditary lineage of homosexuals for it to manifest. It’s quite reasonable to assume that for currently misunderstood biochemical reasons, it has appeared regularly and consistently throughout human societies, with its openness (rather than occurrence) affected by the prevailing morality of the day. An alternate interpretation of “novel” which requires an unhealthy dose of casuistry is to consider things that are maladaptive, and what could be more maladaptive than an attraction to people who cannot bear your children? However, this suggestion is deeply undermined by the fact that homosexuality is evident in hundreds of animal species, even where the sexual behaviour doesn’t seem to be affected by the availability of members of the opposite sex, as with zebra finches. This indicates that homosexuality has an important, though misunderstood biological function, potentially even an adaptive one, that cannot be deemed novel as though only fully sentient beings capable of exploiting the pleasures of unusual sexualities are able to indulge in it. While classical music is not Kanazawa’s specialist field, the sheer irrationality of his music claims are worthy of even greater embarrassment. His argument here teeters on the shaky foundation that classical music can be defined as instrumental music, and non-classical music as music with vocals. There are so many things wrong with this that it boggles the mind. First, there are plenty of genres of instrumental music that are not classical and are not as typically intellectually challenging, such as film soundtracks, techno, dance, smooth jazz, and muzak. Plus, a heck of a lot of classical music is vocal. In fact, the history of classical music begins predominantly with vocal music, and the song, or lied, has been a staple of the genre for centuries, not to mention opera. The reason that he even sets up this false dichotomy in the first place is that an appreciation of instrumental music is supposedly more evolutionarily novel, as we have been appreciating vocals for thousands of years. Despite the fact that this blank assertion cannot be proved, it’s fundamentally irrelevant, as what surely matters is the complexity in structure and tonality of the music in question, not the particular timbres being used. If Brahms’s 3rd Symphony were delivered by a barbershop quartet, it would not become suddenly appealing to fans of Beyoncé. Not only that, but his evidence for the link with intelligence is a meagre pair of surveys in which classical music fans scored highly in verbal intelligence. He unjustifiably extrapolates from verbal intelligence to general; ignores the many flaws everybody knows exist with traditional IQ tests; and takes no account of the socio-economic factors that may cause a correlation between higher levels of education and exposure to classical music. Quite apart from the specifics of these assertions is the fact that it is fundamentally incoherent to try to assess any supposedly evolutionarily novel behaviours as valid for study. It’s extremely appealing to point to things like homosexuality and classical music as they guarantee controversy, but what about universal novelties like reading? And would using a microwave signify greater intelligence given that homo erectus most likely went without ready-meals? This kind of empty pontification seems to have unfortunately come to typify much of the talk that goes on in evolutionary psychology (though I would never rubbish the entire field), and it’s a great shame, as what could have been an area of immense intrigue is being overrun by pseudoscientists with a social or political axe to grind. ——————————————— Satoshi Kanazawa, Kaja Perina (2011). Why More Intelligent Individuals Like Classical Music Behavioral Decision Making : 10.1002/bdm.730...

Satoshi Kanazawa, Kaja Perina. (2011) Why More Intelligent Individuals Like Classical Music. Behavioral Decision Making. info:/10.1002/bdm.730

Exercise in the Treatment of Anxiety and Depression

2012-05-22T12:27:25Z

Regular exercise appears to moderate the severity of anxiety and depression symptoms. However there are few studies that examine the effectiveness of community-based exercise intervention programs for anxiety and depression.One of the largest research studies of this type was recently published in the Journal of Epidemiology and Community Health. This study from Wales examined the effect of an exercise program intervention in a group of inactive community subjects with coronary heart disease, mild to moderate anxiety or depression. Over 2000 subjects participated in the randomized clinical trial.The active exercise intervention program included:Initial consultation with an exercise professionalIntroduction to a fitness facility with motivational interviewing and goal settingIndividual training or group exercise access at a reduced rate (one pound per session, approximately $1.60 in U.S. currency)Telephone contact every four weeks during first 16 weeks with the exercise professional followed by a personal direct consultation at 16 weeks after entryPhone contact by the exercise professional at 8 months followed by an direct assessment at 12 months following entryThe control group received a brief written handout on exercise and continuation of usual care by their primary care physician. The primary outcome measure at 12 months was a recent 7-day physical activity recall and the Hospital Anxiety and Depression Scale score.The active exercise intervention group had higher number of weekly exercise minutes at 12 months compared to the control group (mean of 200 minutes per week compared to 165 minutes in the control group).Physical activity levels increased with the active intervention group in those subjects referred with coronary artery disease alone but not for those referred for anxiety, depression or those referred with coronary artery disease and anxiety or depression. Despite no increase in activity level in those referred with anxiety and depression, 12 month anxiety and depression scale scores did decline more in the intervention group compared to controls. The declines were statistically significant but relatively small in effect (mean change less than one point on both the anxiety and depression scales).Some interesting patterns of response to the exercise intervention were noted in the study. Subjects in the 45 to 59 year old age group showed the largest effect on weekly exercise with younger and older age groups showing limited change. Additionally, women showed the greatest response to the intervention. Weekly exercise duration in men at 12 months did not differ by intervention assignment, although both men intervention groups had approximately the same weekly exercise minute totals as the women in the active intervention group. The authors note the reduction in anxiety and depression scores in the active intervention may be due to the personal attention and social support of the exercise professional rather than an increase in physical activity levels. This study highlights one of the problems with the use of exercise in the treatment of anxiety and depression. Individuals with anxiety and depression are less likely to adhere to a prescribed program of exercise. Further research will be needed to determine methods to increase compliance in these populations. More intense trainer interactions may be necessary to increase compliance rates and fully experience the beneficial effects of exercise on anxiety and depression symptom reduction.Photo of sunset at Lake Itasca State Park in Minnesota from the author's files. Murphy, S., Edwards, R., Williams, N., Raisanen, L., Moore, G., Linck, P., Hounsome, N., Din, N., & Moore, L. (2012). An evaluation of the effectiveness and cost effectiveness of the National Exercise Referral Scheme in Wales, UK: a randomised controlled trial of a public health policy initiative Journal of Epidemiology & Community Health DOI: 10.1136/jech-2011-200689...

Murphy, S., Edwards, R., Williams, N., Raisanen, L., Moore, G., Linck, P., Hounsome, N., Din, N., & Moore, L. (2012) An evaluation of the effectiveness and cost effectiveness of the National Exercise Referral Scheme in Wales, UK: a randomised controlled trial of a public health policy initiative. Journal of Epidemiology . DOI: 10.1136/jech-2011-200689

First Panic Attack and Agoraphobia

2012-05-21T11:52:07Z

Panic disorder commonly presents acutely with a first severe panic attack. Many patients can distinctly remember their first attack even years after the onset of the disorder.Agoraphobia may complicate panic disorder. The word agoraphobia stems from the Greek word "agora" meaning gathering place. The Greek agora was the common area for public assembly. People with agoraphobia commonly fear situations where they may be in a crowd of people. They often fear that in such situations a panic attack may occur and they will be unable to escape. In the modern world, common settings for agoraphobia are crowded buses, airplanes or motor vehicles.Not all individuals with panic disorder develop agoraphobia. It is unclear why this pattern exists. Agoraphobia does tend to occur with more severe and chronic panic disorder. Individuals with relative few and mild panic attacks are less likely to develop agoraphobia.A recent clinical research study from Japan suggests that the place where the first panic attack occurs may play a role in the risk of developing panic disorder. Hara and colleagues studied a large group (n=830) of individuals with panic disorder and classified them into 5 groups based on the site of their first panic attack. These five sites were:homeschool or officedriving a carpublic transportationoutside of homeIndividuals experiencing their first panic attack while driving or using public transportation had higher rates of agoraphobia. The rank order for agoraphobia rates by site of first panic attack were: public transportation (61%), driving a car (56%), outside of home (49%), school or office (41%) and home (37%).Although individuals experiencing their first panic attack at home had lower rates of agoraphobia they exhibited other markers of severity. They had higher rates of endorsement of the symptom of "fear of dying". Additionally, individuals experiencing their first panic attack at home rated the severity of their first panic attack higher than the other 4 groups.This study supports exploration of the setting and severity of the first panic attack in the assessment of panic disorder. First panic attack setting may contribute to the pattern clinical symptoms and risk of agoraphobia.Photo of black bear and yearling cub from Itasca State Park from the author's files.Hara N, Nishimura Y, Yokoyama C, Inoue K, Nishida A, Tanii H, Okada M, Kaiya H, & Okazaki Y (2012). The development of agoraphobia is associated with the symptoms and location of a patient's first panic attack. BioPsychoSocial medicine, 6 (1) PMID: 22494552...

Hara N, Nishimura Y, Yokoyama C, Inoue K, Nishida A, Tanii H, Okada M, Kaiya H, & Okazaki Y. (2012) The development of agoraphobia is associated with the symptoms and location of a patient's first panic attack. BioPsychoSocial medicine, 6(1), 12. PMID: 22494552

Repetitive brain injury from high impact sports generates similar pathophysiology to traumatic brain injury in soldiers blown up by IEDs

2012-05-21T08:08:12Z

Several retired American Football stars have ended up with chronic traumatic encephalophy (CTE), previously known as dementia pugilistica. It’s similar to Alzheimer’s disease in that the brain ends up with neurofibrillary tangles. CTE has also been seen in soldiers who … Continue reading →...

Goldstein, L., Fisher, A., Tagge, C., Zhang, X., Velisek, L., Sullivan, J., Upreti, C., Kracht, J., Ericsson, M., Wojnarowicz, M.... (2012) Chronic Traumatic Encephalopathy in Blast-Exposed Military Veterans and a Blast Neurotrauma Mouse Model. Science Translational Medicine, 4(134), 134-134. DOI: 10.1126/scitranslmed.3003716