Pub Date : 2026-01-02DOI: 10.1038/s41583-025-01008-y
Linda J Richards, Cheng Huang, Adam Q Bauer, Jin-Moo Lee
Brain function requires exquisitely adapted plasticity at multiple scales, from synapses to whole-brain networks. Evidence for large-scale plasticity in functional brain networks comes from neuroimaging data across a variety of species, particularly during development and following injury. However, how large-scale network remodelling is achieved at the microscopic level is unknown as the growth of entirely new long-distance axons is unlikely to occur. Recent insights from electron microscopic connectome studies and single-cell projectomes of neurons in the brains of multiple model organisms have provided new evidence for the incredible structural complexity of axons and their branches that traverse the brain. This evidence shows highly arborized axonal projections, differentially myelinated branches of the same axon, and axonal regions devoid of synaptic contacts but with the potential to form synaptic connections in new or additional areas. Recent electron microscopic data suggest that these axonal features may be evolutionarily conserved. Here we consider whether these features could enable long-range and large-scale neuroplastic changes at a functional level, particularly following focal brain injury. These insights contribute to our emerging understanding of how the brain undergoes large-scale reorganization to adapt to changing circumstances.
{"title":"Long-range axon branching: contributions to brain network plasticity and repair.","authors":"Linda J Richards, Cheng Huang, Adam Q Bauer, Jin-Moo Lee","doi":"10.1038/s41583-025-01008-y","DOIUrl":"https://doi.org/10.1038/s41583-025-01008-y","url":null,"abstract":"<p><p>Brain function requires exquisitely adapted plasticity at multiple scales, from synapses to whole-brain networks. Evidence for large-scale plasticity in functional brain networks comes from neuroimaging data across a variety of species, particularly during development and following injury. However, how large-scale network remodelling is achieved at the microscopic level is unknown as the growth of entirely new long-distance axons is unlikely to occur. Recent insights from electron microscopic connectome studies and single-cell projectomes of neurons in the brains of multiple model organisms have provided new evidence for the incredible structural complexity of axons and their branches that traverse the brain. This evidence shows highly arborized axonal projections, differentially myelinated branches of the same axon, and axonal regions devoid of synaptic contacts but with the potential to form synaptic connections in new or additional areas. Recent electron microscopic data suggest that these axonal features may be evolutionarily conserved. Here we consider whether these features could enable long-range and large-scale neuroplastic changes at a functional level, particularly following focal brain injury. These insights contribute to our emerging understanding of how the brain undergoes large-scale reorganization to adapt to changing circumstances.</p>","PeriodicalId":19082,"journal":{"name":"Nature Reviews Neuroscience","volume":" ","pages":""},"PeriodicalIF":26.7,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1038/s41583-025-01012-2
Javier Sánchez Romero, Marta Navarrete
Our understanding of memory and learning has been largely overshadowed by neurocentric studies, leaving non-neuronal cells out of the equation. The cellular substrate for memory is thought to lie within engrams - ensembles of neurons that activate during learning, whose reactivation leads to recall of the acquired memory. Astrocytes are now taking centre stage in the modulation of memory and other cognitive functions. Contrary to widespread assumptions, these glial cells activate as sparse groups, or ensembles, and reactivation of astrocyte ensembles recruited during learning produces recall. Recent advances using activity-dependent tools to interrogate the roles of astrocytes in memory support a paradigm shift: engrams not only are composed of neurons but also include astrocyte ensembles that activate during learning, forming what we call 'astroengrams'. Thus, the coordinated activity of neuronal and astrocytic engrams provides an integrated framework to orchestrate memory storage and recall.
{"title":"Astroengrams: rethinking the cellular substrate for memory.","authors":"Javier Sánchez Romero, Marta Navarrete","doi":"10.1038/s41583-025-01012-2","DOIUrl":"https://doi.org/10.1038/s41583-025-01012-2","url":null,"abstract":"<p><p>Our understanding of memory and learning has been largely overshadowed by neurocentric studies, leaving non-neuronal cells out of the equation. The cellular substrate for memory is thought to lie within engrams - ensembles of neurons that activate during learning, whose reactivation leads to recall of the acquired memory. Astrocytes are now taking centre stage in the modulation of memory and other cognitive functions. Contrary to widespread assumptions, these glial cells activate as sparse groups, or ensembles, and reactivation of astrocyte ensembles recruited during learning produces recall. Recent advances using activity-dependent tools to interrogate the roles of astrocytes in memory support a paradigm shift: engrams not only are composed of neurons but also include astrocyte ensembles that activate during learning, forming what we call 'astroengrams'. Thus, the coordinated activity of neuronal and astrocytic engrams provides an integrated framework to orchestrate memory storage and recall.</p>","PeriodicalId":19082,"journal":{"name":"Nature Reviews Neuroscience","volume":" ","pages":""},"PeriodicalIF":26.7,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-11DOI: 10.1038/s41583-025-01000-6
Valerie Y H van Weperen,Marmar Vaseghi
Bidirectional, multilevel communication between the heart and the brain is pivotal for the beat-to-beat regulation of cardiac function and the close titration of cardiac output to meet metabolic demand. Given this bidirectional communication, it is perhaps not surprising that cardiac pathologies lead to changes in the central and peripheral autonomic nervous system, which in turn lead to further progression of cardiovascular disease. Within the CNS, structural and functional changes have been reported in the setting of hypertension and heart failure in multiple autonomic regions and nuclei, including the spinal cord, brainstem, hypothalamus and higher centres, such as the amygdala and thalamus. These alterations enhance the excitability of sympathetic neuronal populations and diminish the excitability of neurons within the parasympathetic nuclei, resulting in sympathovagal imbalance. The primary drivers of these structural and functional changes appear to be a combination of increased angiotensin signalling (both central and peripheral), neuroinflammation, oxidative stress and glial activation. Targeting the CNS in the setting of cardiovascular disease presents an exciting avenue for the field of neuromodulation.
{"title":"The brain-heart axis: effects of cardiovascular disease on the CNS and opportunities for central neuromodulation.","authors":"Valerie Y H van Weperen,Marmar Vaseghi","doi":"10.1038/s41583-025-01000-6","DOIUrl":"https://doi.org/10.1038/s41583-025-01000-6","url":null,"abstract":"Bidirectional, multilevel communication between the heart and the brain is pivotal for the beat-to-beat regulation of cardiac function and the close titration of cardiac output to meet metabolic demand. Given this bidirectional communication, it is perhaps not surprising that cardiac pathologies lead to changes in the central and peripheral autonomic nervous system, which in turn lead to further progression of cardiovascular disease. Within the CNS, structural and functional changes have been reported in the setting of hypertension and heart failure in multiple autonomic regions and nuclei, including the spinal cord, brainstem, hypothalamus and higher centres, such as the amygdala and thalamus. These alterations enhance the excitability of sympathetic neuronal populations and diminish the excitability of neurons within the parasympathetic nuclei, resulting in sympathovagal imbalance. The primary drivers of these structural and functional changes appear to be a combination of increased angiotensin signalling (both central and peripheral), neuroinflammation, oxidative stress and glial activation. Targeting the CNS in the setting of cardiovascular disease presents an exciting avenue for the field of neuromodulation.","PeriodicalId":19082,"journal":{"name":"Nature Reviews Neuroscience","volume":"41 1","pages":""},"PeriodicalIF":34.7,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145728418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-11DOI: 10.1038/s41583-025-01003-3
Yeji Kim,Seongjun Park
Neurochemical signalling has emerged as a rapid, versatile and indispensable layer of neural computation, operating alongside electrical activity to shape circuit dynamics, behaviour and disease progression. Decoding these signals in vivo requires sensing platforms that combine spatiotemporal resolution, molecular specificity and anatomical compatibility, capabilities beyond those of traditional sampling methods. Electrochemical technologies, from fast-scan cyclic voltammetry to molecular recognition sensors, deliver subsecond temporal resolution without genetic manipulation, whereas optical approaches using genetically encoded indicators achieve cell-specific measurements with high spatial precision. However, most existing implementations provide only a single sensing function, restricting measurements to a passive chemical dimension and limiting comprehensive or causal circuit analysis. Hybrid systems begin to bridge this gap by coupling stimulation and sensing within unified interfaces, enabling richer interrogation of brain networks. Building on this foundation, transformative multimodal platforms fundamentally expand the boundaries of chemical sensing, overcoming limitations in scope, resolution and accessibility, to enable brain-wide, multianalyte and remote operation. In doing so, they elevate in vivo neurochemical sensing to a frontier discipline, offering unprecedented opportunities to map, decode and therapeutically modulate the chemical logic that underlies cognition, behaviour and pathology.
{"title":"In vivo multimodal neurochemical interfaces for real-time decoding of brain circuit.","authors":"Yeji Kim,Seongjun Park","doi":"10.1038/s41583-025-01003-3","DOIUrl":"https://doi.org/10.1038/s41583-025-01003-3","url":null,"abstract":"Neurochemical signalling has emerged as a rapid, versatile and indispensable layer of neural computation, operating alongside electrical activity to shape circuit dynamics, behaviour and disease progression. Decoding these signals in vivo requires sensing platforms that combine spatiotemporal resolution, molecular specificity and anatomical compatibility, capabilities beyond those of traditional sampling methods. Electrochemical technologies, from fast-scan cyclic voltammetry to molecular recognition sensors, deliver subsecond temporal resolution without genetic manipulation, whereas optical approaches using genetically encoded indicators achieve cell-specific measurements with high spatial precision. However, most existing implementations provide only a single sensing function, restricting measurements to a passive chemical dimension and limiting comprehensive or causal circuit analysis. Hybrid systems begin to bridge this gap by coupling stimulation and sensing within unified interfaces, enabling richer interrogation of brain networks. Building on this foundation, transformative multimodal platforms fundamentally expand the boundaries of chemical sensing, overcoming limitations in scope, resolution and accessibility, to enable brain-wide, multianalyte and remote operation. In doing so, they elevate in vivo neurochemical sensing to a frontier discipline, offering unprecedented opportunities to map, decode and therapeutically modulate the chemical logic that underlies cognition, behaviour and pathology.","PeriodicalId":19082,"journal":{"name":"Nature Reviews Neuroscience","volume":"1 1","pages":""},"PeriodicalIF":34.7,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145728563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-05DOI: 10.1038/s41583-025-01001-5
Mario Carta, Mikkel Vestergaard, James. F. A. Poulet
{"title":"The neuronal circuits and cellular encoding of thermosensation","authors":"Mario Carta, Mikkel Vestergaard, James. F. A. Poulet","doi":"10.1038/s41583-025-01001-5","DOIUrl":"https://doi.org/10.1038/s41583-025-01001-5","url":null,"abstract":"","PeriodicalId":19082,"journal":{"name":"Nature Reviews Neuroscience","volume":"15 1","pages":""},"PeriodicalIF":34.7,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145680119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-28DOI: 10.1038/s41583-025-00997-0
Oleg Butovsky, Neta Rosenzweig, Kilian L. Kleemann, Mehdi Jorfi, Vijay K. Kuchroo, Rudolph E. Tanzi, Howard L. Weiner
{"title":"Immune dysfunction in Alzheimer disease","authors":"Oleg Butovsky, Neta Rosenzweig, Kilian L. Kleemann, Mehdi Jorfi, Vijay K. Kuchroo, Rudolph E. Tanzi, Howard L. Weiner","doi":"10.1038/s41583-025-00997-0","DOIUrl":"https://doi.org/10.1038/s41583-025-00997-0","url":null,"abstract":"","PeriodicalId":19082,"journal":{"name":"Nature Reviews Neuroscience","volume":"11 1","pages":""},"PeriodicalIF":34.7,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145614005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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