Nature Neuroscience provides the international neuroscience community with a highly visible forum in which the most exciting developments in all areas of neuroscience can be communicated to a broad readership. A lively front half, including News & Views, Reviews, Perspectives and editorials, helps place the primary research in context, providing readers with a broad perspective on the entire field. Nature Neuroscience aims to provide readers with authoritative, accessible and timely information on the most important advances in understanding the nervous system. Areas covered include molecular, cellular, systems, behavioral, cognitive and computational studies. http://feeds.nature.com/neuro/rss/current Nature Publishing Group en © 2026 Macmillan Publishers Limited, part of Springer Nature. All rights reserved. Nature Neuroscience © 2026 Macmillan Publishers Limited, part of Springer Nature. All rights reserved. permissions@nature.com https://www.nature.com/uploads/product/neuro/rss.gif http://feeds.nature.com/neuro/rss/current https://www.nature.com/articles/s41593-026-02418-6 Nature Neuroscience, Published online: 08 September 2026; doi:10.1038/s41593-026-02418-6

Although Alzheimer’s disease (AD) is a disease of the brain, we demonstrate that it disrupts myeloid cell production in the bone marrow via a type I interferon signal, preventing protective monocyte-derived macrophages from reaching the brain. Blocking this signal in the 5xFAD mouse model of amyloidosis restored healthy monocyte output and alleviated disease manifestations, highlighting the peripheral immune system as a therapeutic target.]]> doi:10.1038/s41593-026-02418-6 Nature Neuroscience, Published online: 2026-09-08; | doi:10.1038/s41593-026-02418-6 2026-09-08 Nature Neuroscience 10.1038/s41593-026-02418-6 https://www.nature.com/articles/s41593-026-02418-6 https://www.nature.com/articles/s41593-026-02428-4 Nature Neuroscience, Published online: 08 September 2026; doi:10.1038/s41593-026-02428-4

Intestinal CD4+ T cells migrate to the dura and brain following gut infection with bacteria or parasites, establishing a long-lived memory population capable of proliferation and cytokine production following rechallenge with bloodborne pathogens.]]> + T cells in the brain and meninges]]> Aaron FlemingKaren NeishRafael Di Marco-BarrosDavid A. PosnerColin Y. C. LeeAndrew StewartZewen Kelvin TuongMiles BremridgeAna PeñalverMia CabantousNathan RichozAnais PortetKatherine HarcourtEleanor GillmanTammie Tao Min SowTetsuo HasegawaDavid Ruano-GallegoGad FrankelDavid WithersSimon ClareMenna R. Clatworthy doi:10.1038/s41593-026-02428-4 Nature Neuroscience, Published online: 2026-09-08; | doi:10.1038/s41593-026-02428-4 2026-09-08 Nature Neuroscience 10.1038/s41593-026-02428-4 https://www.nature.com/articles/s41593-026-02428-4 https://www.nature.com/articles/s41593-026-02417-7 Nature Neuroscience, Published online: 08 September 2026; doi:10.1038/s41593-026-02417-7

Alzheimer’s disease progression involves reduced bone marrow production of myeloid cells due to type I interferon signaling, which hampers the homing of protective immune cells to the affected brain. In a mouse model, inhibiting this pathway restored immune cell recruitment and halted disease progression.]]> Miguel Angel AbellanasLeyre BasurcoMaitreyee PurnapatreChiara BurgalettoGiulia CastellaniSarah Phoebeluc ColaiutaJavier Maria Peralta-RamosAngham IbraheemSama MuradPaola AntonelloMariangeles KovacsYuliya AndrosovaBar NathansohnHannah PartneyLiora CahalonRafael Valdes-MasJoseph M. JosephidesTomer M. SalameMaria EspelosinMar Cuadrado-TejedorAna Garcia-OstaAleksandra DeczkowskaMichal Schwartz doi:10.1038/s41593-026-02417-7 Nature Neuroscience, Published online: 2026-09-08; | doi:10.1038/s41593-026-02417-7 2026-09-08 Nature Neuroscience 10.1038/s41593-026-02417-7 https://www.nature.com/articles/s41593-026-02417-7 https://www.nature.com/articles/s41593-026-02447-1 Nature Neuroscience, Published online: 07 September 2026; doi:10.1038/s41593-026-02447-1

Implanted brain–computer interfaces hold great promise for restoring communication and other functions and for revealing new aspects of human brain physiology. Yet as the number of implantations in humans expands, ethical clarity must keep pace with technical ambition. We propose that this should involve distinguishing research participation from patient care, ensuring long-term support for study participants, ensuring that research participants do not bear disproportionate risks for benefits realized mainly by others, and grounding research in meaningful clinical purpose.]]> Kai J. MillerDavide GiampiccoloHarith AkramGerwin Schalk doi:10.1038/s41593-026-02447-1 Nature Neuroscience, Published online: 2026-09-07; | doi:10.1038/s41593-026-02447-1 2026-09-07 Nature Neuroscience 10.1038/s41593-026-02447-1 https://www.nature.com/articles/s41593-026-02447-1 https://www.nature.com/articles/s41593-026-02463-1 Nature Neuroscience, Published online: 04 September 2026; doi:10.1038/s41593-026-02463-1

Author Correction: Choroid plexus apocrine secretion shapes CSF proteome during mouse brain development]]> Ya’el CourtneyJoshua P. HeadNeil DaniOlga V. ChechnevaFrederick B. ShipleyYong ZhangMichael J. HoltzmanCameron SadeghTowia A. LibermannMaria K. Lehtinen doi:10.1038/s41593-026-02463-1 Nature Neuroscience, Published online: 2026-09-04; | doi:10.1038/s41593-026-02463-1 2026-09-04 Nature Neuroscience 10.1038/s41593-026-02463-1 https://www.nature.com/articles/s41593-026-02463-1 https://www.nature.com/articles/s41593-026-02442-6 Nature Neuroscience, Published online: 04 September 2026; doi:10.1038/s41593-026-02442-6

Why some skills are easier to learn than others remains a central question in neuroscience. Busch and colleagues demonstrate that the intrinsic geometry of human brain activity shapes learning, thereby facilitating adaptation that remains within existing neural manifolds while limiting learning beyond them.]]> Aaron P. Batista doi:10.1038/s41593-026-02442-6 Nature Neuroscience, Published online: 2026-09-04; | doi:10.1038/s41593-026-02442-6 2026-09-04 Nature Neuroscience 10.1038/s41593-026-02442-6 https://www.nature.com/articles/s41593-026-02442-6 https://www.nature.com/articles/s41593-026-02434-6 Nature Neuroscience, Published online: 04 September 2026; doi:10.1038/s41593-026-02434-6

This study argues that neuromodulation should harness the brain’s natural compensatory adaptations, rather than solely restore healthy-like dynamics, providing a framework for improving cognition in psychiatric and aging populations.]]> Shrey GroverWen WenRobert M. G. Reinhart doi:10.1038/s41593-026-02434-6 Nature Neuroscience, Published online: 2026-09-04; | doi:10.1038/s41593-026-02434-6 2026-09-04 Nature Neuroscience 10.1038/s41593-026-02434-6 https://www.nature.com/articles/s41593-026-02434-6 https://www.nature.com/articles/s41593-026-02427-5 Nature Neuroscience, Published online: 03 September 2026; doi:10.1038/s41593-026-02427-5

The authors identify peripheral dendritic cell priming of T cells as a key driver of brain inflammation and neurodegeneration in a mouse model of tauopathy, providing new insights into immune mechanisms contributing to tau-dependent neurodegeneration.]]> + T cells by peripheral dendritic cells exacerbates tau-mediated neurodegeneration]]> Hao HuPeter Bor-Chian LinCarisa ZengYongyi LiMegan E. BoschJoshua T. EmmersonPrabal SharmaRay A. OharaWendy DongTong WuSiling DuWenqing GaoHong JiangLiya YuanXin BaoShasha LiAnthony N. VomundPetra Erdmann-GilmoreYichen GuMiwei HuJonathan NulmanTimothy M. MillerWayne M. YokoyamaCheryl F. LichtiJeffrey MilbrandtRichard J. PerrinJonathan KipnisMaxim N. ArtyomovKenneth M. MurphyJason D. UlrichDavid M. Holtzman doi:10.1038/s41593-026-02427-5 Nature Neuroscience, Published online: 2026-09-03; | doi:10.1038/s41593-026-02427-5 2026-09-03 Nature Neuroscience 10.1038/s41593-026-02427-5 https://www.nature.com/articles/s41593-026-02427-5