Pub Date : 2025-11-11DOI: 10.1038/s41593-025-02110-1
Aksheev Bhambri, Phu Thai, Songtao Wei, Han-Gyu Bae, Payton Reynolds, Daniela Barbosa, Tripti Sharma, Ze Yu, Chao Xing, Jun Hee Kim, Guoqiang Yu, Lu O. Sun
{"title":"Genetic targeting of premyelinating oligodendrocytes reveals activity-dependent myelination mechanisms","authors":"Aksheev Bhambri, Phu Thai, Songtao Wei, Han-Gyu Bae, Payton Reynolds, Daniela Barbosa, Tripti Sharma, Ze Yu, Chao Xing, Jun Hee Kim, Guoqiang Yu, Lu O. Sun","doi":"10.1038/s41593-025-02110-1","DOIUrl":"https://doi.org/10.1038/s41593-025-02110-1","url":null,"abstract":"","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"6 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145484908","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 : 2025-11-11DOI: 10.1038/s41593-025-02094-y
Lesley R. Golden, Dahlia S. Siano, Isaiah O. Stephens, Steven M. MacLean, Kai Saito, Georgia L. Nolt, Jessica L. Funnell, Akhil V. Pallerla, Sangderk Lee, Cathryn Smith, Jing Chen, Haining Zhu, Clairity Voy, Callie M. Whitus, Gabriela Hernandez, Brandon C. Farmer, Kumar Pandya, Dale O. Cowley, Shannon L. Macauley, Scott M. Gordon, Josh M. Morganti, Lance A. Johnson
Compared to individuals carrying two copies of the ε4 allele of apolipoprotein E (APOE), ε2 homozygotes have an approximate 99% reduction in late-onset Alzheimer’s disease (AD) risk. Here we develop a knock-in model that allows for an inducible ‘switch’ between risk and protective alleles (APOE4s2). Gene expression and proteomic analyses confirm that APOE4s2 mice synthesize E4 at baseline and E2 after tamoxifen administration. A whole-body allelic switch results in a metabolic profile resembling E2/E2 humans and drives AD-relevant alterations in the lipidome and single-cell transcriptome, particularly in astrocytes. Finally, when crossed to the 5xFAD background, astrocyte-specific E4 to E2 switching improves cognition, decreases amyloid pathology, lowers gliosis and reduces plaque-associated apolipoprotein E. Together, these data show that a short-term transition from APOE4 to APOE2 can broadly affect the cerebral transcriptome and lipidome, and that astrocyte-specific APOE replacement may be a viable strategy for future gene editing approaches to simultaneously reduce multiple AD-associated pathologies. Using a mouse model enabling an inducible ‘switch’, Golden et al. show that an astrocyte-specific replacement of the Alzheimer’s risk gene APOE4 with protective APOE2 alters metabolism and gene expression, reducing amyloid pathology and gliosis.
{"title":"APOE4 to APOE2 allelic switching in mice improves Alzheimer’s disease-related metabolic signatures, neuropathology and cognition","authors":"Lesley R. Golden, Dahlia S. Siano, Isaiah O. Stephens, Steven M. MacLean, Kai Saito, Georgia L. Nolt, Jessica L. Funnell, Akhil V. Pallerla, Sangderk Lee, Cathryn Smith, Jing Chen, Haining Zhu, Clairity Voy, Callie M. Whitus, Gabriela Hernandez, Brandon C. Farmer, Kumar Pandya, Dale O. Cowley, Shannon L. Macauley, Scott M. Gordon, Josh M. Morganti, Lance A. Johnson","doi":"10.1038/s41593-025-02094-y","DOIUrl":"10.1038/s41593-025-02094-y","url":null,"abstract":"Compared to individuals carrying two copies of the ε4 allele of apolipoprotein E (APOE), ε2 homozygotes have an approximate 99% reduction in late-onset Alzheimer’s disease (AD) risk. Here we develop a knock-in model that allows for an inducible ‘switch’ between risk and protective alleles (APOE4s2). Gene expression and proteomic analyses confirm that APOE4s2 mice synthesize E4 at baseline and E2 after tamoxifen administration. A whole-body allelic switch results in a metabolic profile resembling E2/E2 humans and drives AD-relevant alterations in the lipidome and single-cell transcriptome, particularly in astrocytes. Finally, when crossed to the 5xFAD background, astrocyte-specific E4 to E2 switching improves cognition, decreases amyloid pathology, lowers gliosis and reduces plaque-associated apolipoprotein E. Together, these data show that a short-term transition from APOE4 to APOE2 can broadly affect the cerebral transcriptome and lipidome, and that astrocyte-specific APOE replacement may be a viable strategy for future gene editing approaches to simultaneously reduce multiple AD-associated pathologies. Using a mouse model enabling an inducible ‘switch’, Golden et al. show that an astrocyte-specific replacement of the Alzheimer’s risk gene APOE4 with protective APOE2 alters metabolism and gene expression, reducing amyloid pathology and gliosis.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 12","pages":"2461-2475"},"PeriodicalIF":20.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41593-025-02094-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145484905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-11DOI: 10.1038/s41593-025-02108-9
Jeff Y. L. Lam, Kai Wang, Guojun Bu
In this issue of Nature Neuroscience, Golden et al. unveil a mouse model that enables in vivo ‘switching’ from the Alzheimer’s risk gene APOE4 to the protective gene APOE2. This genetic conversion reshapes Alzheimer’s disease-related metabolism, reduces neuropathology, and enhances cognition, demonstrating the beneficial effects of APOE genetic targeting as a promising therapeutic strategy.
{"title":"Flipping APOE to reverse Alzheimer’s disease traits","authors":"Jeff Y. L. Lam, Kai Wang, Guojun Bu","doi":"10.1038/s41593-025-02108-9","DOIUrl":"10.1038/s41593-025-02108-9","url":null,"abstract":"In this issue of Nature Neuroscience, Golden et al. unveil a mouse model that enables in vivo ‘switching’ from the Alzheimer’s risk gene APOE4 to the protective gene APOE2. This genetic conversion reshapes Alzheimer’s disease-related metabolism, reduces neuropathology, and enhances cognition, demonstrating the beneficial effects of APOE genetic targeting as a promising therapeutic strategy.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 12","pages":"2407-2409"},"PeriodicalIF":20.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145484909","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 : 2025-11-11DOI: 10.1038/s41593-025-02090-2
Olav B. Smeland, Gleda Kutrolli, Shahram Bahrami, Vera Fominykh, Nadine Parker, Julian Fuhrer, Guy F. L. Hindley, Linn Rødevand, Piotr Jaholkowski, Markos Tesfaye, Pravesh Parekh, Torbjørn Elvsåshagen, Andrew D. Grotzinger, Nils Eiel Steen, Dennis van der Meer, Kevin S. O’Connell, Srdjan Djurovic, Anders M. Dale, Alexey A. Shadrin, Oleksandr Frei, Ole A. Andreassen
Although neurological and psychiatric disorders have historically been considered to reflect distinct pathogenic entities, recent findings suggest shared pathophysiological mechanisms. However, the extent to which these heritable disorders share genetic influences remains unclear. Here we performed a comprehensive analysis of genome-wide association study data, involving nearly 1 million cases across ten neurological diseases and ten psychiatric disorders, to compare their common genetic signal and biological associations. Using complementary statistical tools, we demonstrate that a large set of common genetic variants impacts the risk of multiple neurological and psychiatric disorders, even in the absence of genetic correlations. Furthermore, genome-wide association studies on psychiatric disorders consistently implicate neuronal biology, whereas neurological diseases are associated with diverse neurobiological processes. Together, this study elucidates the genetic relationship between complex neurological and psychiatric disorders, indicating a larger degree of genetic pleiotropy than previously recognized. The findings have implications for disease classification, precision medicine and clinical practice. Smeland et al. demonstrate greater genetic overlap between neurological and psychiatric disorders than previously recognized, along with diverse neurobiological associations. The findings support a more integrated view of brain-related illness.
{"title":"A genome-wide analysis of the shared genetic risk architecture of complex neurological and psychiatric disorders","authors":"Olav B. Smeland, Gleda Kutrolli, Shahram Bahrami, Vera Fominykh, Nadine Parker, Julian Fuhrer, Guy F. L. Hindley, Linn Rødevand, Piotr Jaholkowski, Markos Tesfaye, Pravesh Parekh, Torbjørn Elvsåshagen, Andrew D. Grotzinger, Nils Eiel Steen, Dennis van der Meer, Kevin S. O’Connell, Srdjan Djurovic, Anders M. Dale, Alexey A. Shadrin, Oleksandr Frei, Ole A. Andreassen","doi":"10.1038/s41593-025-02090-2","DOIUrl":"10.1038/s41593-025-02090-2","url":null,"abstract":"Although neurological and psychiatric disorders have historically been considered to reflect distinct pathogenic entities, recent findings suggest shared pathophysiological mechanisms. However, the extent to which these heritable disorders share genetic influences remains unclear. Here we performed a comprehensive analysis of genome-wide association study data, involving nearly 1 million cases across ten neurological diseases and ten psychiatric disorders, to compare their common genetic signal and biological associations. Using complementary statistical tools, we demonstrate that a large set of common genetic variants impacts the risk of multiple neurological and psychiatric disorders, even in the absence of genetic correlations. Furthermore, genome-wide association studies on psychiatric disorders consistently implicate neuronal biology, whereas neurological diseases are associated with diverse neurobiological processes. Together, this study elucidates the genetic relationship between complex neurological and psychiatric disorders, indicating a larger degree of genetic pleiotropy than previously recognized. The findings have implications for disease classification, precision medicine and clinical practice. Smeland et al. demonstrate greater genetic overlap between neurological and psychiatric disorders than previously recognized, along with diverse neurobiological associations. The findings support a more integrated view of brain-related illness.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 12","pages":"2439-2450"},"PeriodicalIF":20.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145484906","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 : 2025-11-11DOI: 10.1038/s41593-025-02105-y
Masakazu Taira, Melissa J. Sharpe
We have all heard the cliché; hormones make us unreliable and unpredictable. However, in this issue of Nature Neuroscience, Golden et al. show that higher states of endogenous estrogen enhance reward prediction errors in sophisticated ways, which promotes adaptive behavior and improves performance.
{"title":"High estrogen states enhance reinforcement learning","authors":"Masakazu Taira, Melissa J. Sharpe","doi":"10.1038/s41593-025-02105-y","DOIUrl":"10.1038/s41593-025-02105-y","url":null,"abstract":"We have all heard the cliché; hormones make us unreliable and unpredictable. However, in this issue of Nature Neuroscience, Golden et al. show that higher states of endogenous estrogen enhance reward prediction errors in sophisticated ways, which promotes adaptive behavior and improves performance.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 12","pages":"2410-2412"},"PeriodicalIF":20.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145484902","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 : 2025-11-11DOI: 10.1038/s41593-025-02104-z
Carla E. M. Golden, Audrey C. Martin, Daljit Kaur, Andrew Mah, Diana H. Levy, Takashi Yamaguchi, Amy W. Lasek, Dayu Lin, Chiye Aoki, Christine M. Constantinople
Gonadal hormones act throughout the brain and modulate psychiatric symptoms. Yet how hormones influence cognitive processes is unclear. Exogenous 17β-estradiol, the most potent estrogen, modulates dopamine in the nucleus accumbens core, which instantiates reward prediction errors (RPEs), the difference between received and expected reward. Here we show that following endogenous increases in 17β-estradiol, dopamine RPEs and behavioral sensitivity to previous rewards are enhanced, and nucleus accumbens core dopamine reuptake proteins are reduced. Rats adjusted how quickly they initiated trials in a task with varying reward states, balancing effort against expected rewards. Nucleus accumbens core dopamine reflected RPEs that influenced rats’ initiation times. Higher 17β-estradiol predicted greater sensitivity to reward states and larger RPEs. Proteomics revealed reduced dopamine transporter expression following 17β-estradiol increases. Finally, knockdown of midbrain estrogen receptors suppressed sensitivity to reward states. Therefore, endogenous 17β-estradiol predicts dopamine reuptake and RPE signaling, and causally dictates the impact of previous rewards on behavior. Dopamine encoding of reward prediction errors naturally fluctuates over females’ reproductive cycles with estrogenic signaling due to reduced expression of dopamine reuptake proteins.
{"title":"Estrogen modulates reward prediction errors and reinforcement learning","authors":"Carla E. M. Golden, Audrey C. Martin, Daljit Kaur, Andrew Mah, Diana H. Levy, Takashi Yamaguchi, Amy W. Lasek, Dayu Lin, Chiye Aoki, Christine M. Constantinople","doi":"10.1038/s41593-025-02104-z","DOIUrl":"10.1038/s41593-025-02104-z","url":null,"abstract":"Gonadal hormones act throughout the brain and modulate psychiatric symptoms. Yet how hormones influence cognitive processes is unclear. Exogenous 17β-estradiol, the most potent estrogen, modulates dopamine in the nucleus accumbens core, which instantiates reward prediction errors (RPEs), the difference between received and expected reward. Here we show that following endogenous increases in 17β-estradiol, dopamine RPEs and behavioral sensitivity to previous rewards are enhanced, and nucleus accumbens core dopamine reuptake proteins are reduced. Rats adjusted how quickly they initiated trials in a task with varying reward states, balancing effort against expected rewards. Nucleus accumbens core dopamine reflected RPEs that influenced rats’ initiation times. Higher 17β-estradiol predicted greater sensitivity to reward states and larger RPEs. Proteomics revealed reduced dopamine transporter expression following 17β-estradiol increases. Finally, knockdown of midbrain estrogen receptors suppressed sensitivity to reward states. Therefore, endogenous 17β-estradiol predicts dopamine reuptake and RPE signaling, and causally dictates the impact of previous rewards on behavior. Dopamine encoding of reward prediction errors naturally fluctuates over females’ reproductive cycles with estrogenic signaling due to reduced expression of dopamine reuptake proteins.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 12","pages":"2502-2514"},"PeriodicalIF":20.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41593-025-02104-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145484907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-10DOI: 10.1038/s41593-025-02174-z
Cagney E. Coomer, Daria Naumova, Mustafa Talay, Bence Zolyomi, Nathaniel J. Snell, Altar Sorkaç, Jean Michel Chanchu, Ji Cheng, Ivana Roman, Jennifer Li, Drew Robson, David L. McLean, Gilad Barnea, Marnie E. Halpern
{"title":"Author Correction: Transsynaptic labeling and transcriptional control of zebrafish neural circuits","authors":"Cagney E. Coomer, Daria Naumova, Mustafa Talay, Bence Zolyomi, Nathaniel J. Snell, Altar Sorkaç, Jean Michel Chanchu, Ji Cheng, Ivana Roman, Jennifer Li, Drew Robson, David L. McLean, Gilad Barnea, Marnie E. Halpern","doi":"10.1038/s41593-025-02174-z","DOIUrl":"10.1038/s41593-025-02174-z","url":null,"abstract":"","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 12","pages":"2647-2647"},"PeriodicalIF":20.0,"publicationDate":"2025-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41593-025-02174-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145478126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-10DOI: 10.1038/s41593-025-02102-1
Haixin Liu, Riccardo Melani, Marta Maltese, James Taniguchi, Akhila Sankaramanchi, Ruoheng Zeng, Jenna R. Martin, Nicolas X. Tritsch
Dopamine (DA) is essential for the production of vigorous actions, but how DA modifies the gain of motor commands remains unclear. Here we show that subsecond DA transients in the striatum of mice are neither required nor sufficient for specifying the vigor of ongoing forelimb movements. Our findings have important implications for our understanding of how DA contributes to motor control under physiological conditions and in Parkinson’s disease. Liu and colleagues show that the vigor (that is, speed and amplitude) of dexterous movements is not controlled by ongoing fluctuations in extracellular dopamine within the dorsal striatum of mice.
{"title":"Subsecond dopamine fluctuations do not specify the vigor of ongoing actions","authors":"Haixin Liu, Riccardo Melani, Marta Maltese, James Taniguchi, Akhila Sankaramanchi, Ruoheng Zeng, Jenna R. Martin, Nicolas X. Tritsch","doi":"10.1038/s41593-025-02102-1","DOIUrl":"10.1038/s41593-025-02102-1","url":null,"abstract":"Dopamine (DA) is essential for the production of vigorous actions, but how DA modifies the gain of motor commands remains unclear. Here we show that subsecond DA transients in the striatum of mice are neither required nor sufficient for specifying the vigor of ongoing forelimb movements. Our findings have important implications for our understanding of how DA contributes to motor control under physiological conditions and in Parkinson’s disease. Liu and colleagues show that the vigor (that is, speed and amplitude) of dexterous movements is not controlled by ongoing fluctuations in extracellular dopamine within the dorsal striatum of mice.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 12","pages":"2432-2438"},"PeriodicalIF":20.0,"publicationDate":"2025-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41593-025-02102-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145478125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-06DOI: 10.1038/s41593-025-02093-z
Natalie Koh, Zhengyu Ma, Abhishek Sarup, Amy C. Kristl, Mark Agrios, Margaret Young, Andrew Miri
When and how motor cortical output directly influences limb muscle activity through descending projections remain poorly resolved, impeding a mechanistic understanding of motor control. Here we addressed this in mice performing an ethologically inspired climbing behavior. We quantified the direct influence of forelimb primary motor cortex (caudal forelimb area) on muscles across the muscle activity states expressed during climbing. We found that the caudal forelimb area instructs muscle activity pattern by selectively activating certain muscles, while less frequently activating or suppressing their antagonists. From Neuropixels recordings, we identified linear combinations (components) of motor cortical activity that covary with these effects. These components differ partially from those that covary with muscle activity and differ almost completely from those that covary with kinematics. Collectively, our results reveal an instructive direct motor cortical influence on limb muscles that is selective within a motor behavior and reliant on a distinct neural activity subspace. Koh, Ma et al. show that during climbing, mouse motor cortex instructs limb muscle activity patterns primarily by selectively activating certain muscles at certain activity states, via neural activity patterns distinct from those previously described.
{"title":"Selective direct influence of motor cortex on limb muscle activity during naturalistic climbing in mice","authors":"Natalie Koh, Zhengyu Ma, Abhishek Sarup, Amy C. Kristl, Mark Agrios, Margaret Young, Andrew Miri","doi":"10.1038/s41593-025-02093-z","DOIUrl":"10.1038/s41593-025-02093-z","url":null,"abstract":"When and how motor cortical output directly influences limb muscle activity through descending projections remain poorly resolved, impeding a mechanistic understanding of motor control. Here we addressed this in mice performing an ethologically inspired climbing behavior. We quantified the direct influence of forelimb primary motor cortex (caudal forelimb area) on muscles across the muscle activity states expressed during climbing. We found that the caudal forelimb area instructs muscle activity pattern by selectively activating certain muscles, while less frequently activating or suppressing their antagonists. From Neuropixels recordings, we identified linear combinations (components) of motor cortical activity that covary with these effects. These components differ partially from those that covary with muscle activity and differ almost completely from those that covary with kinematics. Collectively, our results reveal an instructive direct motor cortical influence on limb muscles that is selective within a motor behavior and reliant on a distinct neural activity subspace. Koh, Ma et al. show that during climbing, mouse motor cortex instructs limb muscle activity patterns primarily by selectively activating certain muscles at certain activity states, via neural activity patterns distinct from those previously described.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"28 12","pages":"2537-2549"},"PeriodicalIF":20.0,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41593-025-02093-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145447225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-06DOI: 10.1038/s41593-025-02103-0
João Pedro Ferrari-Souza, Guilherme Povala, Nesrine Rahmouni, Bruna Bellaver, Pamela C. L. Ferreira, Marco Antônio De Bastiani, Douglas T. Leffa, Firoza Z. Lussier, Cristiano S. Aguzzoli, Wagner S. Brum, Giovanna Carello-Collar, Wyllians V. Borelli, Joseph Therriault, Arthur C. Macedo, Stijn Servaes, Jenna Stevenson, Ilaria Pola, Serge Gauthier, Diogo O. Souza, Lucas Porcello Schilling, Mychael V. Lourenco, Gallen Triana-Baltzer, Hartmuth C. Kolb, Andréa L. Benedet, Nicholas J. Ashton, Dana L. Tudorascu, Henrik Zetterberg, Kaj Blennow, Sterling C. Johnson, Tharick A. Pascoal, Pedro Rosa-Neto, Eduardo R. Zimmer
{"title":"Microglia modulate Aβ-dependent astrocyte reactivity in Alzheimer’s disease","authors":"João Pedro Ferrari-Souza, Guilherme Povala, Nesrine Rahmouni, Bruna Bellaver, Pamela C. L. Ferreira, Marco Antônio De Bastiani, Douglas T. Leffa, Firoza Z. Lussier, Cristiano S. Aguzzoli, Wagner S. Brum, Giovanna Carello-Collar, Wyllians V. Borelli, Joseph Therriault, Arthur C. Macedo, Stijn Servaes, Jenna Stevenson, Ilaria Pola, Serge Gauthier, Diogo O. Souza, Lucas Porcello Schilling, Mychael V. Lourenco, Gallen Triana-Baltzer, Hartmuth C. Kolb, Andréa L. Benedet, Nicholas J. Ashton, Dana L. Tudorascu, Henrik Zetterberg, Kaj Blennow, Sterling C. Johnson, Tharick A. Pascoal, Pedro Rosa-Neto, Eduardo R. Zimmer","doi":"10.1038/s41593-025-02103-0","DOIUrl":"https://doi.org/10.1038/s41593-025-02103-0","url":null,"abstract":"","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":"1 1","pages":""},"PeriodicalIF":25.0,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145447224","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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