Brain Research最新文献

{"title":"Enhancing neuronal viability: The protective role of 10% human cerebrospinal fluid in primary neuronal cultures","authors":"Vineet Arora ,&nbsp;Alicia Bernhardt ,&nbsp;Alessandro Napoli ,&nbsp;Mijail Serruya","doi":"10.1016/j.brainres.2025.149782","DOIUrl":"10.1016/j.brainres.2025.149782","url":null,"abstract":"<div><div>Human cerebrospinal fluid (hCSF) is a physiologically rich medium containing neurotrophic factors, signaling molecules, and essential metabolites that support neuronal development, survival, and function. While its neuroprotective properties have been demonstrated in organotypic brain slices and human iPSC-derived models, its application in primary rodent cortical neuron cultures—a foundational system for studying synaptic development and neurodegeneration—remains underexplored. In this study, we systematically evaluated the effects of hCSF supplementation on neuronal viability in primary cortical cultures derived from embryonic day 18 (E18) rat embryos. To determine the optimal concentration, we tested a range of media:hCSF ratios and identified 90:10 (i.e., 10% hCSF) as the most effective for enhancing neuronal survival. Cell viability was assessed using two complementary assays: SYTOX Green for detecting dead cells and Calcein AM/Ethidium Homodimer-2 (EthD2) dual-staining for quantifying live/dead cell populations. Our results show that 10% hCSF supplementation significantly reduces cell death and improves overall neuronal health under standard in vitro conditions. This optimized approach offers a reproducible and physiologically relevant strategy for improving dissociated cortical neuron cultures and has important implications for in vitro modeling of neurodegenerative diseases, neurotoxicity screening, and regenerative neuroscience research.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1864 ","pages":"Article 149782"},"PeriodicalIF":2.7,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal exercise and neonatal overfeeding induces sex-specific peripheral and brain alterations in the offspring","authors":"Pauline Maciel August ,&nbsp;Bernardo Gindri dos Santos ,&nbsp;Ismael Mesquita ,&nbsp;Alessandra Gonçalves Machado ,&nbsp;Débora Santos Rocha ,&nbsp;Eduardo Z.B. de Assis ,&nbsp;Luisa Soares Pedroso ,&nbsp;Vinicius Stone ,&nbsp;Manuela Menegotto Zeferino ,&nbsp;Carla Dalmaz ,&nbsp;Cristiane Matté","doi":"10.1016/j.brainres.2025.149778","DOIUrl":"10.1016/j.brainres.2025.149778","url":null,"abstract":"<div><div>Childhood obesity is rapidly increasing, resulting in long-term negative health consequences. The impact of early-life factors on adulthood health is described through the Developmental Origin of Health and Disease (DOHaD) concept, which links the metabolic effects of prenatal interventions to an increased risk of chronic non-communicable diseases later in life. Our study aimed to evaluate the influence of prenatal exercise and neonatal overfeeding on pup development, and peripheral metabolic parameters, as well as mitochondrial function and oxidative stress in the hypothalamus and hippocampus. Female Wistar rats were divided into two groups before and during pregnancy: (1) sedentary, and (2) swimming exercise. One day after birth, the litter size was adjusted to 8 pups or 3 pups per dam, leading to control and overfed subgroups within each maternal group. Maternal exercise and neonatal overfeeding resulted in an accelerated eye opening in the pups. Overfeeding-induced increased mesenteric fat in females was decreased by maternal exercise. In male pups, maternal exercise was able to prevent overfeeding-induced increased blood glucose. In the hippocampus we also found a sex-specific effect, with male pups born from exercised dams and raised in an overfeed environment showing impaired mitochondrial function. Overall, our data demonstrates a positive effect of maternal exercise in well-known overweight effects, such as body fat and blood glucose levels. In the male pup hippocampus, maternal exercise could not prevent the sex-specific effects caused by neonatal overfeeding.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1864 ","pages":"Article 149778"},"PeriodicalIF":2.7,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autism spectrum disorders and the volume of the striatum and Amygdala: A Mendelian randomization study","authors":"Zhili Yu ,&nbsp;Zhihao Luo ,&nbsp;Jialing Zheng ,&nbsp;Liming Lu ,&nbsp;Chunzhi Tang ,&nbsp;Chongzheng Qu","doi":"10.1016/j.brainres.2025.149781","DOIUrl":"10.1016/j.brainres.2025.149781","url":null,"abstract":"<div><h3>Backgrounds/Aims</h3><div>A number of studies have documented alterations in the structure and function of the striatum in individuals diagnosed with autism spectrum disorder (ASD). Nevertheless, the precise genetic mechanisms underpinning the relationship between autism spectrum disorder (ASD) and striatum and amygdala volume remain to be elucidated. The objective of this study was to estimate the causal effect of ASD on striatum and amygdala volume.</div></div><div><h3>Methods</h3><div>Summarized data of genome-wide association studies (GWAS) were separately downloaded from the IEU (Integrative Epidemiology Unit) open GWAS project (22138 participants of Europeans (100%), 18,382 cases of ASD and 27,969 controls, with a total of 33,219 brain imaged samples), the Enhancing Neuroimaging Genetics through Meta-Analysis Consortium (ENIGMA) (15640 participants of Europeans (96.5%) and non-Europeans). The MR-egger intercept test, MR-presso and Cochran’s Q statistic was used to examine the pleiotropy and heterogeneity, respectively. MR-egger, weighted median, inverse variance weighted, simple mode, and weighted mode methods were used to evaluate the causal association between striatum and amygdala volume and ASD. Finally, the effect of a single SNP (single nucleotide polymorphism) was used to test the SNP bias.</div></div><div><h3>Results</h3><div>The increased change rate of the putamen shows a strong and statistically significant association with ASD risk (P_IVW = 0.015, P_FDR = 0.044), with a large beta value (β(SE) = 8.272(3.401), 95 %CI: 1.605 to 14.939) indicating a substantial effect size. This makes it a potentially important changes caused by ASD. However, the increased change rate of the amygdala shows a positive but not statistically significant association with ASD risk (P_IVW = 0.119, P_FDR = 0.593). The beta value (2.527) is smaller, and the confidence interval includes zero, suggesting that this result is not reliable as a predictor of ASD risk. The other part of GM (grey matter) of striatum and amygdala volume also showed unsignificant result due to small beta values or unsignificant FDR p values.</div></div><div><h3>Conclusions</h3><div>The putamen’s change rate appears to be a significant change caused by ASD which may be a strong predictive capability for ASD risk, while the amygdala’s change rate and GM of striatum and amygdala volume does not show a significant predictive capability in this context. The present study provides evidence of a genetic relationship between ASD and putamen volume. Further investigation is required to elucidate the mechanisms underlying the genetic effect of changes in putamen structure and function on ASD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1864 ","pages":"Article 149781"},"PeriodicalIF":2.7,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systemic sclerosis and its cerebral, neurological, and psychiatric impacts: a narrative review","authors":"Ryan C. Silva ,&nbsp;Josenilda de M. Arruda ,&nbsp;Michelly C. Pereira ,&nbsp;Moacyr J.B.M. Rêgo ,&nbsp;Maira G.R. Pitta ,&nbsp;Michelle M. da Rosa","doi":"10.1016/j.brainres.2025.149779","DOIUrl":"10.1016/j.brainres.2025.149779","url":null,"abstract":"<div><div>Neurological manifestations of Systemic Sclerosis (SSc) encompass psychiatric disorders, peripheral neuropathy (PN), and cerebrovascular complications, significantly impacting patient quality of life. Psychological assessments reveal high levels of distress linked to depression, anxiety, fatigue, and cognitive impairment. Although PN is less frequent, its distinct profile in SSc suggests intrinsic disease mechanisms, sometimes presenting as an early symptom. Key features of SSc, including microvascular dysfunction, fibroproliferative processes, and vasculitis, elevate stroke risk through atherosclerosis and vascular calcification. Additionally, oxidative stress plays a central role in neural damage, with Reactive Oxygen Species (ROS) contributing to neurological symptoms. This review highlights the diverse neurological outcomes of SSc, underscoring the need for integrative management strategies that address overlooked comorbidities and optimize patient care.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1864 ","pages":"Article 149779"},"PeriodicalIF":2.7,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corydalis yanhusuo Polysaccharides regulates HPA-axis mediated microglia activation and inhibits astrocyte A1 transformation to improve depression-like behavior","authors":"Yu Fang ,&nbsp;Yanqing Li ,&nbsp;Shumin Wang ,&nbsp;Jie Deng ,&nbsp;Jingtao Liang ,&nbsp;Siman Li ,&nbsp;Dongdong Yang ,&nbsp;Bohua Yan","doi":"10.1016/j.brainres.2025.149780","DOIUrl":"10.1016/j.brainres.2025.149780","url":null,"abstract":"<div><div>Depression is a common emotional disorder characterized by persistent low mood and decreased interest. <em>Corydalis yanhusuo</em> polysaccharides (CYP) are extracts from <em>Corydalis yanhusuo</em>, which have the effects of promoting blood circulation, relieving pain, anti-inflammation, and neuroprotection. This study investigates the effects and its underlying mechanisms of CYP in a chronic unpredictable mild stress (CUMS)-induced depression model using C57BL/6J mice. After 4 weeks of CYP treatment, the depressive behavior of mice was observed, and Nissl staining, H&amp;E staining, and immunofluorescence were performed. The hypothalamic–pituitary–adrenal (HPA) axis factors levels were determined by enzyme-linked immunosorbent assay. Western blotting was used to detect protein expression. The results showed that CYP treatment improved depression-like behaviors in mice that received CUMS and ameliorated pathological damage the hippocampus and synaptic damage via regulating the expression of NeuN, SYP, and PSD95 proteins. CYP also reduced neuroinflammation by decreasing the expression of IL-1β, IL-18, NLRP3, and Caspase-1. In addition, CYP reduced adrenocorticotropic hormone (ACTH), corticotropin-releasing hormone (CRH), corticosterone (CORT), corticotropin releasing factor (CRF), mineralocorticoid receptor (MR) levels, and increased glucocorticoid receptor (GR) levels. Furthermore, CYP could regulate microglial activation and transform A1 astrocytes into neuroprotective A2 astrocytes, thereby mitigating neuronal damage by decreasing the expression of complement C3 (C3) and ionized calcium-binding adaptor molecule 1 (Iba-1), while increasing the expression of S100A10. However, CORT treatment significantly reversed above changes and aggravated depressive behavior in mice. In conclusion, CYP could improve CUMS-induced depression-like behaviors by regulating HPA axis-mediated microglial activation and inhibiting A1 transformation of astrocytes.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1864 ","pages":"Article 149780"},"PeriodicalIF":2.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144272632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in blood pressure response to continuous acute Ang II infusion: are only sex hormones to blame?","authors":"Florencia Dadam ,&nbsp;Gabriela V. Silva ,&nbsp;Cintia Y. Porcari ,&nbsp;Andrea Godino ,&nbsp;Laura Vivas ,&nbsp;Ximena E. Caeiro","doi":"10.1016/j.brainres.2025.149740","DOIUrl":"10.1016/j.brainres.2025.149740","url":null,"abstract":"<div><div>The aim of our study was to dissociate sex chromosome complement (SCC), organizational and activational hormonal effects on sexually dimorphic blood pressure regulation during continuous acute Ang-II infusion and on femoral artery Agtr1b receptor gene expression. Transgenic mice of the “four core genotypes” (in which SCC, organizational and activational hormonal effects can be dissociated), were gonadectomized and then divided into (a) without hormone replacement (GDX) (b) with β-estradiol (GDX + E2), and (c) testosterone propionate replacement (GDX + TP) groups. In anesthetized mice percentage changes in blood pressure during continuous Ang-II infusion were assayed during 10 min and (b) femoral artery Agtr1b mRNA expression was evaluated.</div><div>The analysis of mean arterial pressure (MAP) in response to Ang-II infusion revealed an interaction of SCC, organizational and activational-hormonal effects. In GDX mice, while no changes in MAP were observed in XY-Male/GDX mice, it resulted in an increase in XX-Male/GDX, XX-Female/GDX and XY-Female/GDX.</div><div>In XX-Male/GDX + E2, XX-Female/GDX + E2, XY-Female/GDX + E2 an activational depressor β-estradiol effect was observed when compared to GDX groups. GDX + TP treated mice showed an opposite profile to that reported for GDX groups; demonstrating an activational testosterone pressor effect in XY-Male/GDX + TP. Furthermore, an activational hormonal effect on femoral artery Agtr1b gene expression was described; in which, irrespectively of biological sex and SCC, TP groups were demonstrated to show lower Agtr1b expression when compared to GDX and GDX + E2 groups.</div><div>Our data may contribute to the understanding of blood pressure regulation in the complex interplay between RAS, differential SCC backgrounds, the organizational and activational sex hormonal effects.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1863 ","pages":"Article 149740"},"PeriodicalIF":2.7,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trophic factors and essential oils as potential neuromodulators of Renin-Angiotensin system","authors":"Rosana Crespo ,&nbsp;Sol Angulo ,&nbsp;Lucía Nigro ,&nbsp;Rocío Bartolozzi ,&nbsp;Claudia Hereñú","doi":"10.1016/j.brainres.2025.149777","DOIUrl":"10.1016/j.brainres.2025.149777","url":null,"abstract":"<div><div>The renin-angiotensin system (RAS) is a well-established endocrine system primarily recognized for its role in electrolyte homeostasis, fluid balance, and cardiovascular regulation in peripheral circulation. In addition to the systemic RAS, the brain harbors a local and independent RAS.</div><div>Accumulating evidence indicates a close association between the renin-angiotensin system (RAS) and neuroinflammation. This report underscores the pathophysiology role of RAS in neurodegeneration and evaluates its potential as a therapeutic target.</div><div>Growth factors and essential oil have been widely studied for their antioxidant therapeutic potential in inflammatory disorders and other pathologies. Studies on the administration of these molecules have been tested for their potential to provide neuroprotection and stop or slow the progression of neurodegenerative diseases. As a result of these searches, we suggest that growth factors and essential oils neuroprotective effects may be mediated, at least in part, by their interactions with the RAS system influencing neurovascular and neuroinflammatory processes.</div><div>This review intends to summarize and provide evidence to guide future research on the effects of growth factors and essential oils on brain RAS components and their potential therapeutic applications in neuroprotection.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1863 ","pages":"Article 149777"},"PeriodicalIF":2.7,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis and its contribution to cognitive impairment in Alzheimer’s disease: mechanisms and therapeutic potential","authors":"Gyas Khan ,&nbsp;Md Sadique Hussain ,&nbsp;Yumna Khan ,&nbsp;Rabab Fatima ,&nbsp;Sarfaraz Ahmad ,&nbsp;Ayesha Sultana ,&nbsp;Prawez Alam","doi":"10.1016/j.brainres.2025.149776","DOIUrl":"10.1016/j.brainres.2025.149776","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is a progressive neurodegenerative disorder featuring cognitive impairment with loss of memory, with implications of Amyloid-β plaques and hyperphosphorylated tau tangles. Recent studies suggest that ferroptosis, an iron-dependent form of cell death characterized by the accumulation of lipid peroxides, may play a key role in the molecular and cellular pathways underlying neurodegeneration in AD. Dysregulation of iron stability is correlated to oxidative pressure and neuronal damage, especially within the hippocampus and cortex region, promoting a vicious cycle of neurodegeneration. This review focuses on summarizing major recent findings on ferroptosis towards cognitive impairment in AD involving major regulatory genes such as HIF1α and GPX4, in neuroprotection or as a risk factor of the disease. The predictive power of gene expression models based on autopsies and blood samples further highlights the importance of ferroptosis-related pathways, such as autophagy, which influences iron homeostasis and lipid degradation, and mTOR signaling, which regulates oxidative stress responses and cell survival, in shaping AD pathology and progression. Moreover, the review sheds light on novel therapeutic strategies targeting ferroptosis, such as ferroptosis inhibitors, iron chelation, and several antioxidant therapies, which hold promise for alleviating cognitive deficits and advance treatment paradigms in AD. Investigating the role of ferroptosis in AD may uncover new therapeutic strategies that target the interconnected processes of cognitive decline and neurodegeneration.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1864 ","pages":"Article 149776"},"PeriodicalIF":2.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144263761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Nrf2-GPX4 axis mitigates ferroptosis-driven early brain injury in experimental subarachnoid hemorrhage","authors":"Jian Zhou,&nbsp;Haowen Zhang,&nbsp;Yao Wang,&nbsp;Qiuhu Huang","doi":"10.1016/j.brainres.2025.149761","DOIUrl":"10.1016/j.brainres.2025.149761","url":null,"abstract":"<div><div>Subarachnoid hemorrhage (SAH) is a catastrophic cerebrovascular event often resulting from the rupture of intracranial aneurysms, leading to significant brain damage and lasting neurological deficits. Despite advancements in treatment, the mechanisms underlying early brain injury (EBI) following SAH, particularly the role of ferroptosis, remain poorly understood. This study aims to elucidate the impact of Nrf2- glutathione peroxidase 4 (GPX4) pathway on ferroptosis in EBI after experimental SAH. Male Sprague-Dawley rats were subjected to prechiasmatic cistern SAH, with interventions involving Nrf2 modulation using ML385 (a specific inhibitor) or resveratrol (an activator). The results demonstrate that SAH significantly increases iron content, lipid reactive oxygen species (ROS), and malondialdehyde levels while reducing glutathione levels and suppressing GPX4 expression, which promotes ferroptosis. Resveratrol significantly decreases iron content, lipid ROS, and MDA levels; increases GPX4 expression; and restores mitochondrial morphology, whereas the Nrf2 inhibitor ML385 causes opposite changes in these metrics. These findings highlight the crucial role of the Nrf2-GPX4 pathway in regulating ferroptosis following SAH, which suggests it as a potential therapeutic target for mitigating EBI.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1863 ","pages":"Article 149761"},"PeriodicalIF":2.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144262785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Irregular temporal fluctuations in visual, cognitive and emotional brain regions in primary open-angle glaucoma patients","authors":"Qian Wang ,&nbsp;Bingbing Yang ,&nbsp;Xiaoxia Qu ,&nbsp;Zihan Chai ,&nbsp;Ting Li ,&nbsp;Yunxiao Sun ,&nbsp;Junfang Xian","doi":"10.1016/j.brainres.2025.149775","DOIUrl":"10.1016/j.brainres.2025.149775","url":null,"abstract":"<div><div>Primary open-angle glaucoma (POAG) is now seen as a progressively worsening neurodegenerative disorder. Previvors neuroimaging studies neglect dynamic brain activity, assuming static patterns in resting-state functional MRI (rs-fMRI), while intrinsic brain activity is dynamic and fluctuates over time. To test the time-varying brain activity in POAG patients, a temporal dynamic analysis of rs-fMRI data was conducted on 70 POAG patients and 45 healthy controls (HCs). The sliding-window method calculated dynamic amplitude of low-frequency fluctuations (dALFF) across the brain, and group differences and correlations with ophthalmological and neuropsychological measures were analyzed. Multivariate pattern analysis evaluated dALFF and static-ALFF’s ability to differentiate POAG patients from HCs. POAG patients exhibited lower dALFF in visual network areas and higher dALFF in the default mode, ventral attention, and frontoparietal networks compared to HCs. Decreased dALFF in the cuneus correlated with visual field deficits. Visual network dALFF distinguished POAG patients from HCs with 79.13 % accuracy, 66.67 % sensitivity, and 87.14 % specificity (<em>p</em> = 0.001). The dALFF’s area under the curve was significantly greater than that of static-ALFF (<em>p</em> = 0.026). POAG patients show irregular time-varying brain activity, especially in areas linked to vision, movement, and emotional/cognitive functions. This study suggests that dALFF offers a novel approach to capture the aberrant time-varying brain activity and its clinical relation, holding potential for enhancing the understanding of POAG mechanisms and improving its diagnosis.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1863 ","pages":"Article 149775"},"PeriodicalIF":2.7,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}