ASN NEURO最新文献

{"title":"Border-Associated Macrophages in CNS Health and Disease: A Comprehensive Review of Ontogeny, Heterogeneity, and Functional Plasticity at Neural Interfaces.","authors":"Xueting Liu, Mingyue Li, Zengrong Wei, Tong Shang, Wei Zou","doi":"10.1080/17590914.2026.2687503","DOIUrl":"10.1080/17590914.2026.2687503","url":null,"abstract":"<p><p>Border-associated macrophages (BAMs) represent a specialized population of tissue-resident immune cells strategically positioned at the critical interfaces between the central nervous system (CNS) and peripheral circulation, including the meninges, choroid plexus, and perivascular spaces. As frontline sentinels of the neuroimmune system, BAMs perform essential functions in immune surveillance, barrier integrity maintenance, and homeostatic regulation, yet their unique biology and disease-associated roles remain incompletely characterized compared to parenchymal microglia. This review aims to synthesize current knowledge on BAM ontogenetic origins, compartment-specific heterogeneity, transcriptional programs, and functional outputs in both health and neurological disorders. We conducted a comprehensive literature analysis integrating findings from lineage tracing studies, single-cell RNA sequencing, spatial transcriptomics, and functional interrogation in animal models of disease. The results reveal that BAMs exhibit remarkable cellular diversity shaped by distinct ontogenetic origins-primarily yolk sac-derived erythro-myeloid progenitors with variable contributions from fetal liver and postnatal monocytes depending on anatomical compartment. Compartment-specific marker combinations (CD206, LYVE1, CD163, MHCII) define functionally distinct subsets, and core transcriptional regulators including PU.1 and IRF8 maintain BAM identity while CSF-1/IL-34-CSF1R signaling governs survival and renewal. In neurological disorders including ischemic stroke, Alzheimer's disease, multiple sclerosis, and brain tumors, BAMs display pronounced double-edged roles, transitioning from protective homeostatic guardians to pathogenic drivers depending on disease stage and microenvironmental context. This comprehensive analysis establishes a unified framework for understanding BAM biology and identifies critical opportunities for developing subset-specific therapeutic strategies targeting these interface macrophages in neurological diseases.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2687503"},"PeriodicalIF":4.4,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13336290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GABA Receptor Activation in Müller Glia as a Molecular Switch for Controlling VEGF-A in the Retina.","authors":"Alan E Medina-Arellano, Jesus Silvestre Albert-Garay, Karla Tovar-Hernandez, Matilde Ruiz-Cruz, Lenin Ochoa-de la Paz","doi":"10.1080/17590914.2026.2618997","DOIUrl":"10.1080/17590914.2026.2618997","url":null,"abstract":"<p><p>GABA receptors are classically known for driving neuronal hyperpolarization and modulating synaptic transmission. In glial cells, however, GABA induces depolarization and triggers calcium-dependent signaling pathways. Müller glia, the principal retinal glial population, maintain retinal homeostasis and are the major source of neuroretinal VEGF-A, a key angiogenic factor in development and disease. Although GABA receptor (GABAR) activity has been proposed to influence retinal VEGF-A, it remains unclear whether this regulation occurs through Müller glial cells (MGC) and which mechanisms are involved. Here, we investigated how GABAR activation modulates VEGF-A in primary mouse MGC cultures. Cells were exposed to GABA and selective agonists or antagonists of GABA_A (muscimol, gabazine) and GABA_B receptors (baclofen, CGP55845). VEGF-A expression and secretion were analyzed by immunofluorescence, western blot, RT-qPCR, and ELISA. To assess Ca²⁺ involvement, we used Ca²⁺-free Ringer-Krebs solution and the L-type channel blocker nimodipine, and examined MAPK signaling with the ERK1/2 inhibitor FR180204. Our findings show that GABA and muscimol increased VEGF-A fluorescence intensity after 48 hours while reducing VEGF-A secretion, without altering <i>Vegfa</i> mRNA. Both effects were abolished by extracellular Ca²⁺ removal or nimodipine, indicating a Ca²⁺-dependent mechanism. FR180204 also attenuated GABA- and GABA_A-mediated effects, implicating MAPK signaling. Short-term assays revealed that GABA rapidly elevates VEGF-A protein and secretion within ∼30 minutes. Together, these findings identify a Ca²⁺- and GABA_A-dependent pathway through which Müller glia regulate VEGF-A production and release, providing new insight into glial signaling and neurotransmitter-driven modulation of retinal angiogenic factors.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2618997"},"PeriodicalIF":4.4,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disrupted Vitamin D Signaling and Metabolism in Neurodevelopmental and Neurodegenerative Disorders.","authors":"Nasim Khatibi, Jessica L MacDonald","doi":"10.1080/17590914.2026.2617453","DOIUrl":"10.1080/17590914.2026.2617453","url":null,"abstract":"<p><p>Vitamin D is a secosteroid hormone with myriad physiological functions, including pleiotropic effects in the central nervous system. Vitamin D deficiency has been linked to multiple neurodevelopmental and neurodegenerative diseases, including Rett syndrome, epilepsy, Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Over the past decades, vitamin D supplementation has been used as a preventative measure or a therapeutic intervention, often with inconsistent or variable responses. We discuss the known association between vitamin D deficiency and neurological disorder occurrence or progression for these disorders. Further, we assess the underlying causes for disruptions in vitamin D levels and the potential mechanisms of vitamin D-mediated improvements. We discuss disruptions in the vitamin D metabolism pathway, signaling, and/or feedback homeostasis that could underpin individual responses to vitamin D supplementation in these disorders. We further discuss the intersection between the vitamin D and cholesterol synthesis pathways and neuroinflammation, and the complex interactions that could contribute to the broad impact of vitamin D on neurological disorders.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2617453"},"PeriodicalIF":4.4,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha-Synuclein Dynamics in Cerebral Ischemia.","authors":"Sanaz Bordbar, Sina Molavizade, Fateme Dehghani, Samin Davoody, Amir Reza Bahadori, Abbas Tafakhori","doi":"10.1080/17590914.2026.2615453","DOIUrl":"10.1080/17590914.2026.2615453","url":null,"abstract":"<p><p>Cerebral ischemia is defined by insufficient blood supply to the brain and is a leading cause of mortality and neurological disability worldwide. Alpha-synuclein (α-Syn) is a protein associated with several neurodegenerative disorders, including Parkinson's disease, and has also been linked to the pathophysiology of cerebral ischemia. This narrative review provides a detailed overview of the current understanding of α-Syn in cerebral ischemia. We examine its impact on neuroinflammation, synaptic dysfunction, oxidative stress, and neuronal cell death, as well as its potential protective roles. Additionally, we explore therapeutic strategies targeting α-Syn, including pharmacological agents, gene knockdown models, and RNA-based therapies. We also discuss α-Syn expression changes in animal and human studies and its potential as a diagnostic biomarker. By clarifying the complex interplay between α-Syn and cerebral ischemia, this review aims to deepen our understanding of ischemic brain injury mechanisms and support the development of novel treatment approaches.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2615453"},"PeriodicalIF":4.4,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Thy1 in Cortico-Striatal Pathways Alters Response to Dopamine and Gabapentin.","authors":"Cezar Goletiani, Matthew D McEchron, Elizabeth Neely, James R Connor","doi":"10.1080/17590914.2026.2615452","DOIUrl":"10.1080/17590914.2026.2615452","url":null,"abstract":"<p><p>Thy1, a synaptic protein, may support synaptic junction adherence. Thus, we hypothesized that loss of Thy1 may alter synaptic transmission. Our focus on the Thy1 knockout (KO) mouse model stems from the loss of Thy1 expression in individuals with Restless Legs Syndrome (RLS), a neurological disorder. This investigation aimed to determine: 1) if the absence of Thy1 affects synaptic function in the striatal region, 2) if the absence of Thy1 alters the synaptic response to dopamine and gabapentin, and 3) if the Thy1 loss can alter behavior modulated by the striatum. Network-level synaptic transmission was measured in corticostriatal slices from Thy1 KO and C57BL/6 control mice. <i>In vivo</i>, acoustic startle behavioral testing was used to measure startle reaction and prepulse inhibition in both groups. Raclopride, a D₂ receptor antagonist, decreased population spike amplitude in control but not Thy1 KO slices. Quinpirole, a D₂ receptor agonist, did not change spike amplitude in any group. Gabapentin, a Ca²⁺ channel blocker, reduced population spike amplitude in Thy1 KO slices more than in controls. The behavioral acoustic startle response was diminished in Thy1 KO mice and attributed to enhanced prepulse inhibition. Loss of Thy1 alters striatal synaptic function, affecting dopaminergic modulation of corticostriatal neurotransmission and resulting in disruption of the startle response and prepulse inhibition.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2615452"},"PeriodicalIF":4.4,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12818806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145987818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shared Transcriptomic and Epigenomic Signatures Between Traumatic Brain Injury and Music Exposure: An Integrative Proof of Concept.","authors":"Alberto Gómez-Carballa, Sara Pischedda, Nour El Zahraa Mallah, Wiktor Nowak, Federico Martinón-Torres, Laura Navarro, Antonio Salas","doi":"10.1080/17590914.2026.2691563","DOIUrl":"10.1080/17590914.2026.2691563","url":null,"abstract":"<p><p>Music-based interventions have shown promise in aiding recovery in individuals with brain damage (BD), including acquired and traumatic brain injury (ABI and TBI). To investigate the underlying molecular mechanisms, we conducted a study integrating transcriptomic and epigenomic data. We compared gene expression changes driven by musical stimuli in healthy individuals exposed to music with transcriptomic data from TBI patients, identifying 154 common differentially expressed genes (DEGs) affected in TBI and impacted by music, including <i>STK35</i>, <i>HNRNPA0</i>. These genes are notably involved in synaptic plasticity, and neurodegenerative processes. Epigenomic analysis revealed that 92 of these DEGs also exhibited significant differential methylation in TBI samples, particularly in genes associated with neurodevelopment, neuroinflammation, and mood regulation. Pathway enrichment and cross-validation in independent datasets of TBI patients highlighted the cGMP-PKG signaling pathway, a key regulator of memory and plasticity. Co-expression network analysis further revealed six gene modules significantly associated with TBI, including modules centered on <i>TXNIP</i> and <i>ALG13</i> genes, previously implicated in neuroinflammation and epilepsy, two conditions commonly associated with TBI. Interestingly, several hub genes from these modules also showed sensitivity to musical stimuli, suggesting that music may target biologically relevant networks involved in TBI pathology. These findings reveal intriguing molecular parallels between signatures associated with TBI and the biological response to music exposure, providing a proof-of-concept for future investigation. This molecular insight suggests a potential role for music as a biologically grounded component of neurorehabilitation. However, future studies should directly assess transcriptomic and epigenomic responses to music-based interventions in BD patients.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2691563"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13502011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148787728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperoxia Inhibits the Growth of Mouse Forebrain Oligodendrocyte Progenitors but Promotes Their Differentiation.","authors":"Lisamarie Moore, Lauren McLane, Stacey Wahl, Isis M Ornelas, Teresa L Wood, Peter Canoll, Steven W Levison","doi":"10.1080/17590914.2026.2698260","DOIUrl":"10.1080/17590914.2026.2698260","url":null,"abstract":"<p><p>Oligodendrocytes facilitate saltatory conduction and they support both neuronal and axonal survival; thus, when they are diseased or damaged, neurological problems ensue. Oligodendrocyte progenitors (OPCs) have been successfully isolated from rodents using magnetic beads, immunopanning and differential adhesion. Whereas rat OPCs are easy to propagate <i>in vitro</i>, expanding mouse OPCs in vitro has not been straightforward, which is problematic given that mice have been used to generate the majority of genetically engineered disease models. In this study, we developed and characterized a reproducible, straightforward method to prepare large numbers of nearly homogeneous cultures of mouse OPCs. Using the McCarthy and de Vellis mechanical separation method, we isolated OPCs from a mixture of glial cells and plated them onto fibronectin-coated tissue culture plates in a biochemically defined medium supplemented with fibroblast growth factor-2 (FGF-2) and medium conditioned by B104 neuroblastoma cells. However, when maintained in a standard tissue culture incubator, they proliferated very slowly and ∼ 20% died. By contrast, when they were maintained in an incubator with 2% oxygen they proliferated more rapidly and could be expanded for multiple passages with high viability. After three passages, greater than 99% of these OPCs expressed markers of early OPCs. In medium containing only FGF-2 they progressed to late-stage OPCs. When a medium supplemented with T3 was provided, a large subset of OPCs differentiated into O4+/MBP+ oligodendrocytes with sheet-like membranes. However, between 3 and 6 passages, less than 20% of the OPCs differentiated into MBP+ oligodendrocytes and this was associated with a loss of Sox-10. These studies reveal significant differences between mouse and rat OPCs and a role for oxygen tension in mouse OPC proliferation and differentiation.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2698260"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13596923/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149007866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to Frontline Antiretroviral Dolutegravir Disrupts Oligodendrocyte Development Across Differentiation Stages.","authors":"Marisa A Jeffries, Raj Putatunda, Melanie Cruz-Berríos, Micah A Romer, Anushka Singhal, Kelly L Jordan-Sciutto, Judith B Grinspan","doi":"10.1080/17590914.2026.2647877","DOIUrl":"10.1080/17590914.2026.2647877","url":null,"abstract":"<p><p>The use of antiretroviral (ART) treatment during pregnancy has dramatically reduced rates of perinatally-acquired human immunodeficiency virus 1 (HIV-1) infection to <1% in the United States. Despite this success, we have limited knowledge of how ART drugs that cross the placental barrier affect fetal development, particularly in the central nervous system (CNS). During gestation, large populations of oligodendroglia are produced that are responsible for critical postnatal CNS myelination enabling appropriate neurological function. Previous studies have shown that antiretrovirals impair oligodendrocyte (OL) differentiation leading us to hypothesize that OL maturation might be inhibited by exposure to a frontline ART drug cocktail (Triumeq®) prescribed during pregnancy containing dolutegravir (DTG), abacavir (ABC), and lamivudine (3TC). In this study, we demonstrated that exposing primary rat oligodendrocyte precursor cells (OPCs) and OLs to the Triumeq drug combination decreased OL maturation and myelin protein production in a concentration-dependent manner, and that DTG was solely responsible. Regardless of the timing of exposure during OL development, a high concentration of DTG inhibited OL maturation. Bulk RNA sequencing revealed transcriptional changes after DTG exposure related to a variety of cellular mechanisms, including cellular responses to stress pathways, amino acid starvation, and mitochondrial dysfunction. Although we found that DTG robustly activated the integrated stress response (ISR), attempted rescue experiments showed that DTG primarily inhibits OL maturation independently of the ISR. Collectively, our novel data on DTG underscore the necessity of investigating how ART drugs that are administered during pregnancy and cross the placental barrier can affect fetal CNS development.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2647877"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13034632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147571912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress in Research on the Mechanisms and Therapeutic Targets of Ferroptosis in Peripheral Nerve Injury and Repair.","authors":"Jian Ruan, Xin-Kun He, Song-Ou Zhang, Xiao-Feng Teng, Yiyang Hu, Hong Chen","doi":"10.1080/17590914.2026.2678168","DOIUrl":"10.1080/17590914.2026.2678168","url":null,"abstract":"<p><p>Repair after peripheral nerve injury (PNI) faces major obstacles due to microenvironmental imbalance and neuronal loss. Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, has emerged as a key pathological event in PNI, linking oxidative stress, mitochondrial dysfunction, and inflammation to regenerative failure. Targeting ferroptosis protects vital cells-such as Schwann cells and neurons-and ameliorates the regenerative niche, offering a promising therapeutic strategy. This review elucidates the mechanisms of ferroptosis in PNI, detailing its roles in Schwann cells, dorsal root ganglion neurons, and macrophages via core pathways including Nrf2/HO-1/GPX4 and ACSL4. We further evaluate current intervention strategies and their therapeutic efficacy. This synthesis provides novel insights into PNI pathology and guides the development of innovative treatments.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2678168"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13217914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148026336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microstructural Features Linking White Matter and Mathematics in Adolescence.","authors":"Bryce L Geeraert, Kiara Kunimoto, R Marc Lebel, Catherine Lebel","doi":"10.1080/17590914.2026.2714165","DOIUrl":"10.1080/17590914.2026.2714165","url":null,"abstract":"<p><p>Mathematics is a complex skill requiring the coordination of distributed gray matter brain regions connected by white matter tracts. Diffusion tensor imaging (DTI) studies have revealed a network of white matter tracts that support math processing, but the specific microstructural features driving this relationship remain unclear. Other magnetic resonance imaging (MRI) methods-neurite orientation dispersion and density imaging (NODDI), inhomogeneous magnetization transfer (ihMT), multicomponent driven-equilibrium single-pulse observation of T1 and T2 (mcDESPOT), and g-ratio imaging-can probe microstructural features like axon packing, fiber orientation, and myelin more specifically than DTI. We applied these methods alongside DTI to evaluate links between white matter microstructure and math in a longitudinal cohort of 33 6-16 year olds (66 datasets total). Partial correlations between metrics of white matter microstructure and math skill, controlling for age and gender, were carried out in the left superior longitudinal and inferior longitudinal fasciculi, corticospinal tract, and the splenium. Cross-sectionally, fiber coherence of the corticospinal tract and superior longitudinal fasciculus correlated to mathematics performance. Longitudinally, change in markers of axonal packing and myelin were linked to changes in both math skill and fluency in a regionally-specific manner, with links to myelin-sensitive metrics most prevalent. Notably, decreases in myelin were linked to improvements in mathematics over time, suggesting ongoing refinement of the math network. Findings presented here did not survive multiple comparisons corrections, but provide insight for future work elaborating upon these associations in larger samples.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2714165"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13471135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}