IBRO Neuroscience Reports最新文献

{"title":"Vitamin D and brain volumetric changes: An updated systematic review and meta-analysis","authors":"Rozhina Tamannaeifar ,&nbsp;Salar Yousefzadeh ,&nbsp;Sana Rahmani ,&nbsp;Maedeh Bayani ,&nbsp;Mahdiyeh Nozad Varjovi ,&nbsp;Nima Eftekhari ,&nbsp;Mona Ranjkesh ,&nbsp;Mahsa Kohansal Vajargah ,&nbsp;Sajjad Hajihosseini ,&nbsp;Faezeh Ahanj ,&nbsp;Hadis Sarlak ,&nbsp;Komeil Aghazadeh-Habashi ,&nbsp;Melika Arab Bafrani ,&nbsp;Alaleh Alizadeh ,&nbsp;Yaser Khakpour ,&nbsp;Niloofar Deravi","doi":"10.1016/j.ibneur.2025.04.011","DOIUrl":"10.1016/j.ibneur.2025.04.011","url":null,"abstract":"<div><h3>Background</h3><div>In this systematic review and meta-analysis, we aimed to investigate the relationship between vitamin D levels and brain volumetric changes in human studies.</div></div><div><h3>Method</h3><div>We conducted a comprehensive search in PubMed, Scopus, and Google Scholar databases up to December 2024. A total of 450 studies were identified. Following title, abstract, and full-text screening, we included three studies for analysis. Data were extracted from these studies and analyzed using appropriate statistical methods.</div></div><div><h3>Result</h3><div>Our analysis revealed that the included case-control and cohort studies were conducted in the United States, Norway, and the Netherlands. The studies exhibited a range of characteristics, including sample size (number of patients: 183–240), demographic variables, and methods of assessing both vitamin D levels and brain volume. Brain volume assessments included gray matter, white matter, and total brain volume. The total follow-up duration across studies was 11 years. The age of participants ranged from 30 to 64 years in one study, while in another, they were aged 65 years or older. The meta-analysis indicated no significant association between vitamin D levels and brain volumetric changes across the included studies (effect size: 0.07, 95 % CI= [-0.01, 0.15], P = 0.07, I²=54.44 %).</div></div><div><h3>Conclusion</h3><div>This meta-analysis did not establish a significant association between vitamin D levels and brain volumetric changes. These findings highlighted the need for further large-scale studies to clarify the potential role of vitamin D in brain volume and to better understand the underlying mechanisms involved.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 844-852"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144185229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the knowledge of epilepsy and Potassium Channels: A scientometric analysis in CiteSpace and VOSviewer","authors":"Zheng Li","doi":"10.1016/j.ibneur.2025.05.004","DOIUrl":"10.1016/j.ibneur.2025.05.004","url":null,"abstract":"<div><div>Epilepsy is one of the most common neurological diseases. Studies have suggested that epileptic seizures are directly related to ion channel abnormalities in the central nervous system. Activation of potassium ion channels may lead to increased cell excitability and abnormal neuronal excitation. Over the past decade, significant progress has been achieved in understanding the potassium ion channel abnormalities related to epilepsy. To facilitate further research, in this paper, we adopted the bibliometrics method (based on Web of Science database) and used CiteSpace and VOSviewer to visualize literature in the field (Potassium Channels-related epilepsy) from 2010 to 2023. A total of 2415 original research and summary papers were included, and the basic situation, subject theme, and knowledge structure evolution were analyzed and discussed step by step from macro to micro perspectives.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 1-16"},"PeriodicalIF":2.0,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144195622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The microbial guardians: Unveiling the role of gut microbiota in shaping neurodegenerative disease","authors":"Nour Abou Izzeddine ,&nbsp;Kawsar Ahmad ,&nbsp;Christine Bacha ,&nbsp;Maria Jabbour ,&nbsp;Mouin Najjar ,&nbsp;Sethrida Salhab ,&nbsp;Hilda E. Ghadieh ,&nbsp;Amjad Kanaan ,&nbsp;Sami Azar ,&nbsp;Ziad Abi Khattar ,&nbsp;Frederic Harb","doi":"10.1016/j.ibneur.2025.05.014","DOIUrl":"10.1016/j.ibneur.2025.05.014","url":null,"abstract":"<div><div>The gut microbiota, a complex community of microorganisms residing in the digestive tract, plays a pivotal role in human health. Recent studies have highlighted its significant impact on neurodegenerative diseases, conditions that pose profound challenges to affected individuals and society at large. This review explores the intricate relationship between gut microbiota and the progression of neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, Huntington’s disease, and Amyotrophic Lateral Sclerosis. We delve into the dynamic ecosystem of gut microbiota, examining factors influencing its composition and the bidirectional communication established via the gut-brain axis. Emerging evidence suggests that gut microbiota can modulate neurodegenerative disease progression through mechanisms including inflammatory responses, production of neuroactive substances, and regulation of neurotransmitters. Furthermore, we discuss the potential therapeutic implications of targeting gut microbiota with probiotics, prebiotics, and postbiotics. While promising, these interventions face challenges and limitations that must be addressed through ongoing research. Understanding the role of gut microbiota in neurodegenerative diseases is crucial for developing innovative therapeutic strategies and improving patient outcomes.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 17-37"},"PeriodicalIF":2.0,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A meta-analysis update evaluating the treatment effects of donepezil alone versus donepezil combined with memantine for Alzheimer's disease","authors":"Sajjad Hajihosseini ,&nbsp;Seyed Amirali Zakavi ,&nbsp;Zahra Farrokhi ,&nbsp;Mahnaz Amanzadeh ,&nbsp;Parham Panahi ,&nbsp;Mina Mahram ,&nbsp;Nima Eftekhari ,&nbsp;Masoud Noroozi ,&nbsp;Mohammad Javad Ebrahimi ,&nbsp;Alaleh Alizadeh ,&nbsp;Pegah Refahi ,&nbsp;Melika Arab Bafrani ,&nbsp;Maral Moafi ,&nbsp;Niloofar Deravi","doi":"10.1016/j.ibneur.2025.05.016","DOIUrl":"10.1016/j.ibneur.2025.05.016","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer's disease (AD) remains a significant global health problem, with ongoing debates about the most effective treatment approach. While donepezil monotherapy has been traditionally used, recent interest has focused on combining it with memantine. This updated meta-analysis aimed to compare the efficacy of donepezil monotherapy versus its combination with memantine for treating AD.</div></div><div><h3>Method</h3><div>A literature search was conducted in the PubMed, Scopus, and Google Scholar databases up to February 14, 2024. Randomized controlled trials (RCTs) comparing donepezil monotherapy with donepezil combined with memantine in AD patients were included. The quality of each selected study was assessed using the Joanna Briggs Institute (JBI) risk-of-bias tool. Data on cognitive function, measured using the Mini-Mental State Examination (MMSE) and the Severe Impairment Battery (SIB), were extracted and analyzed using a random-effects model.</div></div><div><h3>Results</h3><div>A total of four RCTs, including 1930 patients, met the inclusion criteria. Analysis using a forest plot revealed no significant difference in MMSE scores between monotherapy and combination therapy (OR = 0.54, 95 % CI: 0.06–4.60, p &gt; 0.05). However, SIB scores showed a significant improvement with combination therapy (OR = 7.00, 95 % CI: 1.13–43.24, p &lt; 0.05). Both analyses exhibited high heterogeneity (I² = 72 % for MMSE; I² = 89 % for SIB). The funnel plots suggested minor publication bias for the MMSE outcomes, but some asymmetry was observed in the results for SIB.</div></div><div><h3>Conclusion</h3><div>This meta-analysis suggests that combination therapy with donepezil and memantine significantly benefits patients with severe cognitive impairment, as assessed by the SIB, compared to donepezil monotherapy. However, no significant advantage was observed in MMSE scores. The high heterogeneity among studies highlights the need for cautious interpretation and calls for larger, well-designed randomized controlled trials to further elucidate the comparative efficacy of these two therapeutic approaches in Alzheimer's disease.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 72-82"},"PeriodicalIF":2.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144262212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new two-hit animal model for schizophrenia research: Consequences on social behavior","authors":"Kristina Hakenova ,&nbsp;Anna Mikulecka ,&nbsp;Kristina Holubova ,&nbsp;Marketa Chvojkova ,&nbsp;Romana Slamberova ,&nbsp;Jana Jurcovicova ,&nbsp;Barbora Cechova ,&nbsp;Silvester Ponist ,&nbsp;Jiri Horacek ,&nbsp;Karel Vales","doi":"10.1016/j.ibneur.2025.05.012","DOIUrl":"10.1016/j.ibneur.2025.05.012","url":null,"abstract":"<div><div>Schizophrenia, a profoundly impactful neuropsychiatric disorder, has been the subject of extensive research using animal models. However, certain important aspects remain understudied, including assumed long-term consequences of psychotic episodes on negative symptoms development and progression. Addressing these limitations, we proposed a novel animal model in male rats based on early postnatal immune activation triggered by lipopolysaccharide (LPS), serving as the predisposing factor (1st hit). As the 2nd hit, representing psychotic-like episodes, we implemented a multi-episodic co-treatment with dizocilpine (MK-801) and amphetamine (AMP), spanning multiple developmental periods. The animals were tested in two social behavioral assays in adolescence and adulthood to investigate whether a social deficit would arise. In addition, we evaluated the level of oxytocin (OT), a neuropeptide relevant to social behavior, in selected brain regions. In the social interaction test, when animals could freely interact in the open field and express their social behavioral profile entirely, social behavior decreased in adolescent experimental animals. In the social approach test in the Y maze, all animals, irrespective of treatment, preferred conspecific over an indifferent object and novel rat over a familiar rat. Further, the results revealed that the OT content in the hypothalamus increased with age. In the proposed model, social interaction in the open field was decreased in adolescent but not in adult rats, indicating that the pharmacological manipulations caused only transient age-dependent changes. The study was thus in certain aspects successful in creating a novel approach to model social deficit potentially relevant to schizophrenia; other findings require further investigation.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 38-49"},"PeriodicalIF":2.0,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CHPG's role in regulating apoptosis in heat-stressed microglia through endoplasmic reticulum stress: A new perspective☆","authors":"Yan-xuan He ,&nbsp;Zhi-qiang Zhang ,&nbsp;Xin-xin Zheng ,&nbsp;Fan Huang ,&nbsp;Guoxin He ,&nbsp;Xi-chong Yu ,&nbsp;An-cong Xu","doi":"10.1016/j.ibneur.2025.05.011","DOIUrl":"10.1016/j.ibneur.2025.05.011","url":null,"abstract":"<div><h3>Objective</h3><div>This study aims to explore the influence of microglia-mediated endoplasmic reticulum (ER) stress on cell apoptosis during heat stroke. Understanding this is important as it may help develop new therapies for heat-induced cellular damage and protect glial cells and brain health.</div></div><div><h3>Methods</h3><div>BV-2 cells were used as a cell model for this study. The negative control group was kept at 37°C throughout the experiment. Cells in the experimental group were pretreated with 1 mM CHPG (a selective mGluR5 agonist) for 0.5 hours, followed by heat shock (HS) for 0.5 hours at 40°C and then further cultivation at 37°C for 12 hours. The positive control cells underwent same condition except for drug pretreatment. Several assays were used including CCK8 assay for cell viability, flow cytometry for cell apoptosis index, immunofluorescence for the expression of GRP78, CHOP, and Caspase-12, as well as Western blotting for detecting the protein expression level of GRP78, CHOP, and Caspase-12.</div></div><div><h3>Results</h3><div>Heat shock induced a significant release of endoplasmic reticulum-related proteins and increased the expression levels of GRP78, CHOP, and Caspase-12 in BV-2 cells. CHPG was found to inhibit endoplasmic reticulum stress and cell apoptosis.</div></div><div><h3>Conclusion</h3><div>CHPG may primarily participate in heat shock by mediating endoplasmic reticulum stress and affecting microglia apoptosis.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 823-829"},"PeriodicalIF":2.0,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When Wernicke’s encephalopathy mimics stroke: A case report of atypical thalamic involvement","authors":"Govind Singh Mann MBBS ,&nbsp;Neeti Ajay Gupta MD ,&nbsp;Nitin Jain MD, DM","doi":"10.1016/j.ibneur.2025.05.006","DOIUrl":"10.1016/j.ibneur.2025.05.006","url":null,"abstract":"<div><div>Wernicke’s Encephalopathy (WE) is a metabolic disorder caused by thiamine deficiency, most commonly linked to chronic alcohol use. It typically presents with a triad of ataxia, mental confusion, and oculomotor abnormalities, with classic MRI findings showing symmetric hyperintensities in the mammillary bodies, thalamus, and periaqueductal region. The authors report a case of a 55-year-old male with WE presenting atypical unilateral thalamic hyperintensities on MRI, initially misdiagnosed as ischemic stroke. Delayed thiamine supplementation led to significant clinical improvement and resolution of atypical findings, with subsequent emergence of traditional bilateral WE changes on MRI. This case emphasizes the importance of early thiamine therapy and demonstrates that treatment can still be beneficial even when delayed.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 50-53"},"PeriodicalIF":2.0,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144212844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of neuroinflammation on the progression of Alzheimer’s disease and its significant ramifications for novel anti-inflammatory treatments","authors":"Pritam Kamila ,&nbsp;Koyel Kar ,&nbsp;Sailee Chowdhury ,&nbsp;Priyanka Chakraborty ,&nbsp;Ria Dutta ,&nbsp;Sowmiya S ,&nbsp;Ankul Singh S ,&nbsp;Bhupendra Gopalbhai Prajapati","doi":"10.1016/j.ibneur.2025.05.005","DOIUrl":"10.1016/j.ibneur.2025.05.005","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is increasingly recognized as a disorder not solely of amyloid and tau accumulation but also of chronic immune dysregulation. Emerging evidence highlights the critical role of neuroinflammation, characterized by sustained activation of microglia and astrocytes, cytokine release, and inflammasome activation in accelerating AD progression. Genome-wide studies have further identified key inflammatory genes and immune pathways associated with increased disease risk. This review critically evaluates the mechanistic underpinnings of neuroinflammation in AD, focusing on glial cell behavior, immune signaling, and their contribution to neuronal dysfunction. Importantly, the review highlights recent advances in anti-inflammatory therapeutic approaches, including modulators of IL-1β, TNF-α, TREM2, and CB2 pathways. By integrating mechanistic and therapeutic insights, this work underscores the potential of immunomodulatory strategies as viable interventions in AD and provides a novel framework for future research in targeted anti-neuroinflammatory treatments.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 771-782"},"PeriodicalIF":2.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside C-K inhibits Aβ oligomer-induced Alzheimer's disease pathology progression by regulating microglia-neuron interactions","authors":"Chenghu Xie ,&nbsp;Cunxin Zhang ,&nbsp;Kefeng Zhang ,&nbsp;Shanshan Zhang","doi":"10.1016/j.ibneur.2025.05.007","DOIUrl":"10.1016/j.ibneur.2025.05.007","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer’s disease is a progressive neurodegenerative disorder. Current therapeutic agents primarily focus on symptom alleviation and fail to effectively halt disease progression. Therefore, there is a need to develop novel therapeutic strategies, particularly those involving natural active compounds with multi-target actions.</div></div><div><h3>Objective</h3><div>To investigate the intervention effects and multi-target regulatory mechanisms of Ginsenoside C-K (GCK) on β-amyloid (Aβ) oligomer-induced Alzheimer's disease (AD) pathological progression.</div></div><div><h3>Methods</h3><div>BV2 microglia and HT22 neurons were used as in vitro models. Cell viability was measured via CCK-8 assay, cell migration ability assessed by scratch assay, and apoptosis rate analyzed using Annexin V/PI dual staining. A conditioned medium (CM) strategy was employed to validate microglia-neuron interactions. Western blot was performed to detect key NF-κB signaling pathway proteins (p-IκBα, p-p65) and inflammatory cytokines (TNF-α, IL-1β).</div></div><div><h3>Results</h3><div>GCK pretreatment significantly ameliorated Aβ₁₋₄₂ oligomer-induced BV2 cell dysfunction (viability recovery rate &gt;80 %, p &lt; 0.01), suppressed pro-inflammatory cytokine secretion (TNF-α reduced by 62.3 %, IL-1β by 57.8 %), and inhibited NF-κB pathway activation (p-IκBα/p-p65 expression downregulated &gt;50 %). In HT22 neurons, GCK directly counteracted Aβ toxicity (apoptosis rate decreased from 38.7 % to 15.2 %) and exerted indirect neuroprotection by modulating microglia-derived conditioned medium (CM2 group showed a 2.1-fold increase in neuronal viability compared to CM1).</div></div><div><h3>Conclusion</h3><div>GCK mitigates AD pathology through dual mechanisms-direct inhibition of Aβ neurotoxicity and indirect regulation of microglial homeostasis-with NF-κB signaling suppression as a core mechanism. This study provides new experimental evidence for natural product-based multi-target AD therapies, though further animal studies are required to validate its in vivo efficacy and safety.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 783-793"},"PeriodicalIF":2.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A study on structural imaging changes and serum neurofilament light chain (NfL) levels in individuals with white matter hyperintensities, combining imaging techniques with biomarker analysis","authors":"Meini Wu ,&nbsp;Zihao Li ,&nbsp;Yuhang Ren ,&nbsp;Siou Li ,&nbsp;Weina Zhao ,&nbsp;Jian Xing ,&nbsp;Jiangnan Yi ,&nbsp;Fengze Zhao ,&nbsp;Changhao Yin","doi":"10.1016/j.ibneur.2025.05.008","DOIUrl":"10.1016/j.ibneur.2025.05.008","url":null,"abstract":"<div><h3>Objective</h3><div>To elucidate the association between serum neurofilament light chain (NfL) levels and structural brain alterations in individuals exhibiting white matter hyperintensities (WMHs), as well as to investigate the potential utility of serum NfL as a predictive biomarker for the progression of WMH.</div></div><div><h3>Methods</h3><div>A total of 151 subjects were included in the study, among whom 117 demonstrated the presence of white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI). We assessed the relationship between changes in serum neurofilament light chain (NfL) levels and alterations in brain volume across three distinct groups. Additionally, we analyzed trends in brain structural changes and serum NfL level variations within the population exhibiting varying severities of WMHs, exploring the correlation between these two variables.</div></div><div><h3>Results</h3><div>Serum NfL levels were significantly elevated in individuals with WMHs compared to those with none-low WMHs (p &lt; 0.001). Furthermore, higher serum NfL levels were observed in individuals with severe-moderate WMHs compared to those with mild WMHs (p &lt; 0.01). Within the mild WMHs group, serum NfL levels exhibited a negative correlation with gray matter volume. In contrast, within the severe to moderate WMHs group, serum NfL levels were negatively correlated with both gray matter volume (GMV) and white matter volume (WMV). Voxel-based morphometry (VBM) analysis indicated the presence of gray matter atrophy in several brain regions when comparing the none-low WMHs group with the severe to moderate WMHs group, as well as when comparing the mild WMHs group with the severe-moderate WMHs group. However, no significant differences were observed in the comparison between the none to low WMHs group and the mild WMHs group.</div></div><div><h3>Conclusion</h3><div>Serum NfL levels have been observed to rise in conjunction with the increasing severity of WMH and show a correlation with gray matter atrophy in individuals exhibiting WMHs. These levels are anticipated to serve as a biological marker for predicting the progression of WMH.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 794-802"},"PeriodicalIF":2.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}