Pub Date : 2026-04-01Epub Date: 2026-01-21DOI: 10.1016/j.conb.2025.103163
Emmanuelle C. Genin , Véronique Paquis-Flucklinger
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the progressive loss of motor neurons. ALS often overlaps clinically and pathologically with frontotemporal dementia (FTD), the second most common form of dementia. Like many neurodegenerative disorders, both ALS and FTD share a crucial pathological hallmark, the aggregation of misfolded proteins into insoluble inclusions in degenerating neurons. This process is referred to as proteinopathy. This review focuses on the proteinopathies associated with ALS, including aggregates of TDP-43, SOD1, FUS, and CHCHD10, which disrupt critical cellular processes such as RNA metabolism, mitochondrial function, and protein homeostasis. The review highlights to the identification of new types of mitochondrial and cytosolic aggregates linked to CHCHD10-related ALS. Although the precise pathological mechanisms remain to be fully elucidated, strategies aimed at restoring proteostasis and reducing protein aggregation may be promising therapeutic approaches for treating ALS, as they directly target fundamental pathogenic mechanisms.
{"title":"ALS-related proteinopathies: From TDP-43 to mitochondrial proteinopathies","authors":"Emmanuelle C. Genin , Véronique Paquis-Flucklinger","doi":"10.1016/j.conb.2025.103163","DOIUrl":"10.1016/j.conb.2025.103163","url":null,"abstract":"<div><div>Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the progressive loss of motor neurons. ALS often overlaps clinically and pathologically with frontotemporal dementia (FTD), the second most common form of dementia. Like many neurodegenerative disorders, both ALS and FTD share a crucial pathological hallmark, the aggregation of misfolded proteins into insoluble inclusions in degenerating neurons. This process is referred to as proteinopathy. This review focuses on the proteinopathies associated with ALS, including aggregates of TDP-43, SOD1, FUS, and CHCHD10, which disrupt critical cellular processes such as RNA metabolism, mitochondrial function, and protein homeostasis. The review highlights to the identification of new types of mitochondrial and cytosolic aggregates linked to <em>CHCHD10</em>-related ALS. Although the precise pathological mechanisms remain to be fully elucidated, strategies aimed at restoring proteostasis and reducing protein aggregation may be promising therapeutic approaches for treating ALS, as they directly target fundamental pathogenic mechanisms.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"97 ","pages":"Article 103163"},"PeriodicalIF":5.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146001741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-04-01Epub Date: 2026-01-21DOI: 10.1016/j.conb.2025.103164
Margaux Teil , Philippe Huot
An important part of the field of experimental pharmacology encompasses the study of the effects of molecules in animals. In the case of Parkinson's disease (PD), animal models have played an invaluable role in refining our understanding of the disease, in characterizing the effect of new compounds on the illness, and in bringing new treatments to the clinic. Indeed, it is now hardly conceivable that a drug would be tested in humans if several parameters pertaining to safety, toxicology, efficacy, etc. had not previously been evaluated in animal models. Quite unfortunately, efficacy in experimental models of PD does not necessarily guarantee positive clinical outcomes. In this article, which primarily focusses on the past five years, we review drugs that entered clinical trials for the treatment of levodopa-induced dyskinesia, parkinsonism, disease modification, and had previously been assessed in animal models of PD. The drugs discussed are buspirone, JM-010, befiradol, mesdopetam, foliglurax, dipraglurant, tavapadon, prasinezumab, cinpanemab, nilotinib, minzasolmin, exenatide, NLY01, liraglutide, lixisenatide, and semaglutide. For each molecule, we examine how previous preclinical studies succeeded or failed in predicting efficacy in clinical trials and discuss possible ways to optimize animal-model design and selection to maximize the probability of translational success.
{"title":"The challenges of experimental pharmacology in identifying novel treatments for Parkinson's disease","authors":"Margaux Teil , Philippe Huot","doi":"10.1016/j.conb.2025.103164","DOIUrl":"10.1016/j.conb.2025.103164","url":null,"abstract":"<div><div>An important part of the field of experimental pharmacology encompasses the study of the effects of molecules in animals. In the case of Parkinson's disease (PD), animal models have played an invaluable role in refining our understanding of the disease, in characterizing the effect of new compounds on the illness, and in bringing new treatments to the clinic. Indeed, it is now hardly conceivable that a drug would be tested in humans if several parameters pertaining to safety, toxicology, efficacy, etc. had not previously been evaluated in animal models. Quite unfortunately, efficacy in experimental models of PD does not necessarily guarantee positive clinical outcomes. In this article, which primarily focusses on the past five years, we review drugs that entered clinical trials for the treatment of levodopa-induced dyskinesia, parkinsonism, disease modification, and had previously been assessed in animal models of PD. The drugs discussed are buspirone, JM-010, befiradol, mesdopetam, foliglurax, dipraglurant, tavapadon, prasinezumab, cinpanemab, nilotinib, minzasolmin, exenatide, NLY01, liraglutide, lixisenatide, and semaglutide. For each molecule, we examine how previous preclinical studies succeeded or failed in predicting efficacy in clinical trials and discuss possible ways to optimize animal-model design and selection to maximize the probability of translational success.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"97 ","pages":"Article 103164"},"PeriodicalIF":5.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146001742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-13DOI: 10.1016/j.conb.2025.103148
Christine Petit , Paul Avan
In mammals, the exquisite sensitivity and frequency selectivity of sound analysis rests on properly timed cycle-by-cycle feedback that compensates for friction and tunes the mechanical resonances of the auditory sensory organ. This feedback must operate at the highest audible frequencies, more than 100 kHz in some species, a feat given that it relies upon voltage-driven conformation changes of a protein called prestin, which forms an array along the lateral membrane of outer hair cell endowing them with electromotility. In the first place, the voltage that actuates prestin results from mechanotransduction of sound-induced vibrations by a mechanosensitive protein complex hosted in hair cell microvilli called stereocilia, whose nanometric deflections must ensure ion channel activation within microseconds. Many molecular assemblies and configurations allowing mechanosensitive detection to be pushed to such physical scales in terms of displacement and time, a unique requirement of hearing among mechanosensory systems, are still under active investigations.
{"title":"Bridging the gap between physics and biology of hearing: Timing and amplification","authors":"Christine Petit , Paul Avan","doi":"10.1016/j.conb.2025.103148","DOIUrl":"10.1016/j.conb.2025.103148","url":null,"abstract":"<div><div>In mammals, the exquisite sensitivity and frequency selectivity of sound analysis rests on properly timed cycle-by-cycle feedback that compensates for friction and tunes the mechanical resonances of the auditory sensory organ. This feedback must operate at the highest audible frequencies, more than 100 kHz in some species, a feat given that it relies upon voltage-driven conformation changes of a protein called prestin, which forms an array along the lateral membrane of outer hair cell endowing them with electromotility. In the first place, the voltage that actuates prestin results from mechanotransduction of sound-induced vibrations by a mechanosensitive protein complex hosted in hair cell microvilli called stereocilia, whose nanometric deflections must ensure ion channel activation within microseconds. Many molecular assemblies and configurations allowing mechanosensitive detection to be pushed to such physical scales in terms of displacement and time, a unique requirement of hearing among mechanosensory systems, are still under active investigations.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"96 ","pages":"Article 103148"},"PeriodicalIF":5.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145748927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-23DOI: 10.1016/j.conb.2025.103151
Xia-Jing Tong , Fei Wang , Xiaohong Xu
In sexually reproducing animals, males and females are biologically specialized to produce sperm or eggs, which must unite through mating to ensure successful reproduction. To facilitate this, each sex displays sex-specific, often stereotyped, mating behaviors orchestrated by neural circuits that undergo sexual differentiation during development. Extensive anatomical mapping and functional dissection in genetically tractable model organisms, including Caenorhabditis elegans, Drosophila melanogaster, and Mus musculus, have revealed many sexually dimorphic neuronal populations and neural circuits. While previous reviews have offered broad cross-species comparisons of such sex differences in the nervous system [1,2], here we take a more focused approach. We specifically examine the neural substrates underlying mating behaviors across these three species, aiming to highlight shared principles in circuit architecture and to advance the emerging concept of connectome sex.
{"title":"Sexually dimorphic neural circuits underlying mating behaviors: Insights from worms, flies, and mice","authors":"Xia-Jing Tong , Fei Wang , Xiaohong Xu","doi":"10.1016/j.conb.2025.103151","DOIUrl":"10.1016/j.conb.2025.103151","url":null,"abstract":"<div><div>In sexually reproducing animals, males and females are biologically specialized to produce sperm or eggs, which must unite through mating to ensure successful reproduction. To facilitate this, each sex displays sex-specific, often stereotyped, mating behaviors orchestrated by neural circuits that undergo sexual differentiation during development. Extensive anatomical mapping and functional dissection in genetically tractable model organisms, including <em>Caenorhabditis elegans</em>, <em>Drosophila melanogaster</em>, and <em>Mus musculus</em>, have revealed many sexually dimorphic neuronal populations and neural circuits. While previous reviews have offered broad cross-species comparisons of such sex differences in the nervous system [<span><span>1</span></span>,<span><span>2</span></span>], here we take a more focused approach. We specifically examine the neural substrates underlying mating behaviors across these three species, aiming to highlight shared principles in circuit architecture and to advance the emerging concept of <em>connectome sex</em>.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"96 ","pages":"Article 103151"},"PeriodicalIF":5.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-18DOI: 10.1016/j.conb.2025.103147
Kathryn L. Todd , Kaitlyn M.L. Cramb , Katherine R. Brimblecombe , Stephanie J. Cragg
{"title":"Corrigendum to “New insights into axonal regulators of dopamine transmission in health and disease” [Curr Op Neurobiol 94 (2025) 103093]","authors":"Kathryn L. Todd , Kaitlyn M.L. Cramb , Katherine R. Brimblecombe , Stephanie J. Cragg","doi":"10.1016/j.conb.2025.103147","DOIUrl":"10.1016/j.conb.2025.103147","url":null,"abstract":"","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"96 ","pages":"Article 103147"},"PeriodicalIF":5.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145793632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-10DOI: 10.1016/j.conb.2025.103144
Floris P. de Lange , Clare Press
Predictive processing frameworks have emphasized the role of forward prediction as a critical ingredient for learning and perceptual inference. We anticipate sensory events that are likely in the future on the basis of past and current sensory events. By comparing these forward predictions against incoming input, we can obtain an accurate estimate of the environment (i.e. perceive) and improve the predictions themselves (i.e. learn). Interestingly however, research in the field of statistical learning has taught us that backward predictive relationships - reflecting the probability of past events given present events - are learnt equally well. This questions the privileged status of forward-looking mechanisms. Here we discuss commonalities and differences between implications for learning and perception. We conclude that while forward and backward predictive relationships both shape learning, we retrieve future, but not past, predicted states during perception.
{"title":"Forward and backward prediction in learning and perception","authors":"Floris P. de Lange , Clare Press","doi":"10.1016/j.conb.2025.103144","DOIUrl":"10.1016/j.conb.2025.103144","url":null,"abstract":"<div><div>Predictive processing frameworks have emphasized the role of forward prediction as a critical ingredient for learning and perceptual inference. We anticipate sensory events that are likely in the future on the basis of past and current sensory events. By comparing these forward predictions against incoming input, we can obtain an accurate estimate of the environment (i.e. perceive) and improve the predictions themselves (i.e. learn). Interestingly however, research in the field of statistical learning has taught us that backward predictive relationships - reflecting the probability of past events given present events - are learnt equally well. This questions the privileged status of forward-looking mechanisms. Here we discuss commonalities and differences between implications for learning and perception. We conclude that while forward and backward predictive relationships both shape learning, we retrieve future, but not past, predicted states during perception.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"96 ","pages":"Article 103144"},"PeriodicalIF":5.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145721302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-19DOI: 10.1016/j.conb.2025.103150
Ivette M. Sandoval , Michael F. Salvatore , Fredric P. Manfredsson
The prospect of successful use of gene therapy to treat neurological disorders, including Parkinson’s disease (PD), can be increased by understanding the molecular etiology underlying disease symptoms and neurodegeneration. The major hurdle of safety for gene therapy use in central nervous system disorders has been cleared; with now ∼20 years since the first gene therapy clinical trial for PD, and with a large number of patients having received various treatments, the field has generated a large body of data with an impeccable safety record. As our understanding of the targetable components of disease processes evolves, so too do the tools available to target these processes. Viral vectors based on adeno-associated virus have undergone significant advancements in the last decade, including capsid improvements, enhanced production methods, and recombinant genome design. Although the etiopathology(ies) underlying PD is (are) yet to be defined, a number of therapeutic modalities with broad preclinical support have been, and are being, tested in humans. This includes proteins providing symptomatic relief, neuromodulation, monogenic correction, and neurotrophic support. The leading therapeutic gene therapy candidate has been glial cell line–derived neurotrophic factor (GDNF) or the closely related protein neurturin. Although clinical studies are still ongoing, recent work shows that protein levels of GDNF receptors (GDNF family receptor alpha1 and receptor tyrosine kinase) decrease with disease. Therefore, it is possible that optimal use of gene therapy using GDNF, and other protective pathways, can only be realized with an incisive assessment of all components of a targeted signaling pathway. Nevertheless, current clinical candidates, paired with a strong upcoming preclinical data pipeline, are setting the stage for an exciting future for PD gene therapy.
{"title":"Gene therapy for Parkinson’s disease—Ample room for optimism","authors":"Ivette M. Sandoval , Michael F. Salvatore , Fredric P. Manfredsson","doi":"10.1016/j.conb.2025.103150","DOIUrl":"10.1016/j.conb.2025.103150","url":null,"abstract":"<div><div>The prospect of successful use of gene therapy to treat neurological disorders, including Parkinson’s disease (PD), can be increased by understanding the molecular etiology underlying disease symptoms and neurodegeneration. The major hurdle of safety for gene therapy use in central nervous system disorders has been cleared; with now ∼20 years since the first gene therapy clinical trial for PD, and with a large number of patients having received various treatments, the field has generated a large body of data with an impeccable safety record. As our understanding of the targetable components of disease processes evolves, so too do the tools available to target these processes. Viral vectors based on adeno-associated virus have undergone significant advancements in the last decade, including capsid improvements, enhanced production methods, and recombinant genome design. Although the etiopathology(ies) underlying PD is (are) yet to be defined, a number of therapeutic modalities with broad preclinical support have been, and are being, tested in humans. This includes proteins providing symptomatic relief, neuromodulation, monogenic correction, and neurotrophic support. The leading therapeutic gene therapy candidate has been glial cell line–derived neurotrophic factor (GDNF) or the closely related protein neurturin. Although clinical studies are still ongoing, recent work shows that protein levels of GDNF receptors (GDNF family receptor alpha1 and receptor tyrosine kinase) decrease with disease. Therefore, it is possible that optimal use of gene therapy using GDNF, and other protective pathways, can only be realized with an incisive assessment of all components of a targeted signaling pathway. Nevertheless, current clinical candidates, paired with a strong upcoming preclinical data pipeline, are setting the stage for an exciting future for PD gene therapy.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"96 ","pages":"Article 103150"},"PeriodicalIF":5.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-12-20DOI: 10.1016/j.conb.2025.103159
Nolwenn Adam, Jessica Tollkuhn
Social behaviors are crucial for reproductive success and survival. In vertebrates, these behaviors are sexually dimorphic due to distinct hormonal environments in development and adulthood. The underlying neural pathways, collectively known as the social behavior network (SBN), consist of interconnected regions exhibiting sex-variable genomic, anatomical, and functional characteristics. While the structure and function of the adult SBN is increasingly well described, its embryonic origins and development remain poorly understood. All neural networks undergo extensive genomic and functional changes during development, but a unique feature of the SBN is its sensitivity to gonadal hormones. Transient developmental hormone signaling ultimately results in anatomic SBN sexual dimorphism and sex-variable behavioral repertoires. However, the precise mechanisms linking early life hormone signaling to the establishment of neural sex differences remain elusive. This review highlights recent findings on SBN development spanning embryonic timepoints to puberty, offering valuable perspectives to address this critical topic.
{"title":"Development of the social behavior network","authors":"Nolwenn Adam, Jessica Tollkuhn","doi":"10.1016/j.conb.2025.103159","DOIUrl":"10.1016/j.conb.2025.103159","url":null,"abstract":"<div><div>Social behaviors are crucial for reproductive success and survival. In vertebrates, these behaviors are sexually dimorphic due to distinct hormonal environments in development and adulthood. The underlying neural pathways, collectively known as the social behavior network (SBN), consist of interconnected regions exhibiting sex-variable genomic, anatomical, and functional characteristics. While the structure and function of the adult SBN is increasingly well described, its embryonic origins and development remain poorly understood. All neural networks undergo extensive genomic and functional changes during development, but a unique feature of the SBN is its sensitivity to gonadal hormones. Transient developmental hormone signaling ultimately results in anatomic SBN sexual dimorphism and sex-variable behavioral repertoires. However, the precise mechanisms linking early life hormone signaling to the establishment of neural sex differences remain elusive. This review highlights recent findings on SBN development spanning embryonic timepoints to puberty, offering valuable perspectives to address this critical topic.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"96 ","pages":"Article 103159"},"PeriodicalIF":5.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01Epub Date: 2025-11-28DOI: 10.1016/j.conb.2025.103143
Beatriz Maio , Francesca Aria , Susana R. Louros , Emily K. Osterweil
The careful regulation of the protein lifecycle is important for cellular function, particularly during times of change. In neurons, the specializations needed to maintain the steady-state proteome at multiple subcellular domains and respond rapidly to activity have brought about unique mechanisms in messenger RNA (mRNA) translation and protein degradation. Recent research continues to illuminate these critical mechanisms, giving us a deeper understanding of the nervous system and identifying new targets for the treatment of neurological disorders. In this review, we highlight the new research shedding light on the mechanisms of proteostasis in brain development and plasticity. These studies emphasize the extent to which protein synthesis and degradation participate in brain function and how disruptions of proteostasis lead to disorders of the nervous system.
{"title":"Mechanisms of proteostasis in neuronal development and plasticity","authors":"Beatriz Maio , Francesca Aria , Susana R. Louros , Emily K. Osterweil","doi":"10.1016/j.conb.2025.103143","DOIUrl":"10.1016/j.conb.2025.103143","url":null,"abstract":"<div><div>The careful regulation of the protein lifecycle is important for cellular function, particularly during times of change. In neurons, the specializations needed to maintain the steady-state proteome at multiple subcellular domains and respond rapidly to activity have brought about unique mechanisms in messenger RNA (mRNA) translation and protein degradation. Recent research continues to illuminate these critical mechanisms, giving us a deeper understanding of the nervous system and identifying new targets for the treatment of neurological disorders. In this review, we highlight the new research shedding light on the mechanisms of proteostasis in brain development and plasticity. These studies emphasize the extent to which protein synthesis and degradation participate in brain function and how disruptions of proteostasis lead to disorders of the nervous system.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"96 ","pages":"Article 103143"},"PeriodicalIF":5.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145610610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}