Journal of neuroimmunology最新文献

{"title":"The activation of classical and/or lectin complement pathway for the pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy","authors":"Keishu Murakami ,&nbsp;Hiroshi Tsujimoto ,&nbsp;Yoshiaki Nakayama ,&nbsp;Hiroki Takeuchi ,&nbsp;Kenji Yamamoto ,&nbsp;Kei-Ichi Katayama ,&nbsp;Yusuke Inada ,&nbsp;Yutaka Inaba ,&nbsp;Masatoshi Jinnin ,&nbsp;Nobuyuki Oka ,&nbsp;Norimitsu Inoue ,&nbsp;Katsuichi Miyamoto","doi":"10.1016/j.jneuroim.2025.578848","DOIUrl":"10.1016/j.jneuroim.2025.578848","url":null,"abstract":"<div><h3>Background</h3><div>Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a heterogeneous immune-mediated neuropathy. The activation of the complement system has been implicated in CIDP, but it remains unclear which complement pathway activation is essential for the pathogenesis of CIDP. We therefore examined the deposition and production of several activated complement factors in tissues and serum of CIDP, respectively.</div></div><div><h3>Methods</h3><div>We immunohistochemically stained C4d, C3c, and C5b-9 using sural nerve specimens of CIDP and controls. Images were evaluated for the density and fluorescence intensity of complement factor deposition. Serum complement factors (factor H, Ba, sC5b-9, C3, C4 and CH50) were measured in CIDP and in controls. We also investigated clinical data in relation to complement deposition and serum complement factors.</div></div><div><h3>Results</h3><div>C4d was deposited on the myelin sheaths in all patients with CIDP, with significantly higher density and intensity than in controls. C3c was detected in three of the nine patients with CIDP, while C5b-9 was not detected. Serum levels of sC5b-9 were higher than the normal range in some patients, but no significant differences in serum complement levels were observed between those with CIDP and controls. The C4d density and serum C3 levels were positively correlated with Hughes functional grading scale scores.</div></div><div><h3>Conclusions</h3><div>C4d deposition was observed in all patients with CIDP. Few patients showed the activated terminal pathway. The classical and/or lectin pathways are predominantly involved in CIDP pathogenesis. Sural nerve pathology and activated complement factors in the plasma may be useful for selecting therapeutic agents including C2 inhibitors.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"412 ","pages":"Article 578848"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145839090","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 potential role of S-nitrosoglutathione reductase in astrocyte BAFF expression and B cell activation in experimental autoimmune encephalomyelitis","authors":"Jeseong Won ,&nbsp;Judong Kim ,&nbsp;S.M. Touhidul Islam ,&nbsp;Fei Qiao ,&nbsp;Avtar K. Singh ,&nbsp;Inderjit Singh","doi":"10.1016/j.jneuroim.2025.578847","DOIUrl":"10.1016/j.jneuroim.2025.578847","url":null,"abstract":"<div><div>B cell-activating factor (BAFF) is a key mediator of B cell-driven autoimmune pathology. In mice with experimental autoimmune encephalomyelitis (EAE), a widely used model of multiple sclerosis (MS), we observed a pronounced accumulation of B cells within the spinal cord, alongside elevated BAFF expression, particularly in GFAP⁺ activated astrocytes located in the subpial-region. This upregulation of BAFF coincided with the infiltration of CD4⁺ T cells, notably Th1 cells producing IFNγ, a cytokine critical for inducing BAFF gene expression in astrocytes. Concurrently, elevated BAFF levels in the spinal cords of EAE mice were associated with increased expression of S-nitrosoglutathione (GSNO) reductase (GSNOR), the enzyme that degrades GSNO, a molecule known for its anti-inflammatory properties. Pharmacological inhibition of GSNOR using N6022, a reversible inhibitor, significantly reduced BAFF expression and decreased B cell accumulation in the CNS. In vitro, both GSNO and N6022 suppressed IFNγ- and TNFα-induced BAFF expression in cultured astrocytes by inhibiting STAT1 and NF-κB activation. Furthermore, co-culture of B cells with IFNγ/TNFα-stimulated astrocytes, or exposure to their conditioned media, resulted in an increased number of B cells and enhanced IL-6 production. These effects were attenuated either by pretreating astrocytes with GSNO or by applying BAFF-neutralizing antibodies to B cells. Collectively, these findings suggest that GSNOR modulates astrocytic BAFF expression, thereby influencing B cell activation and their IL-6-mediated functions in EAE. Modulation of this pathway may represent a promising avenue for future investigation into immune regulation in MS and related autoimmune conditions.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"412 ","pages":"Article 578847"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145882028","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":"Immune profiling unveils the systemic cytokine milieu associated with acute reversible encephalopathy with cytotoxic lesions of the corpus callosum (CLOCCs)","authors":"Silvia Sperandei ,&nbsp;Lorenzo Gaetani ,&nbsp;Giorgia Manni ,&nbsp;Marco Gargaro ,&nbsp;Giuseppe Vittorio De Socio ,&nbsp;Maria Cristina Gallina ,&nbsp;Andrea Fiacca ,&nbsp;Cinzia Costa ,&nbsp;Andrea Mancini ,&nbsp;Lucilla Parnetti ,&nbsp;Francesca Fallarino ,&nbsp;Massimiliano Di Filippo","doi":"10.1016/j.jneuroim.2025.578834","DOIUrl":"10.1016/j.jneuroim.2025.578834","url":null,"abstract":"<div><div>Encephalopathy with cytotoxic lesions of the corpus callosum (CLOCCs) represents a clinical-radiological entity characterized by MRI evidence of lesions involving the splenium of the corpus callosum and a collection of neurological symptoms ranging from consciousness impairment to seizures and focal neurological signs. The most widely accepted pathophysiological mechanism underlying CLOCCs is thought to be represented by a phenomenon of cytokine-induced cytotoxic edema but its exact immune pathogenesis is still unravelled and targeted treatments are lacking.</div><div>Here, we report the case of a 18-year-old male with CLOCCs associated with acute Epstein-Barr virus (EBV) infection, in whom the systemic immune response across acute and post-acute phases was characterized for the first time through longitudinal cytokine profiling. The obtained data pave the way to a more precise comprehension of CLOCCs pathogenesis and an individualized treatment of this potentially severe condition.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"412 ","pages":"Article 578834"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145771843","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":"Immature ovarian teratomas in anti-NMDA receptor encephalitis","authors":"Kristen Simone ,&nbsp;Nabeela Nathoo ,&nbsp;Allyssa Hooper ,&nbsp;Albert Aboseif ,&nbsp;Andrew Blake Buletko ,&nbsp;Niranjala Satkunam ,&nbsp;Jennifer A. McCombe ,&nbsp;Sophia Pin","doi":"10.1016/j.jneuroim.2025.578850","DOIUrl":"10.1016/j.jneuroim.2025.578850","url":null,"abstract":"<div><div>Anti-<em>N</em>-methyl-<span>d</span>-aspartate receptor autoimmune encephalitis (NMDAR-AIE) is an immune-mediated neurological disease with manifestations including altered mental status, neuropsychiatric disturbance, movement disorders, seizure, and dysautonomia. NMDAR-AIE is associated with ovarian teratoma in half of cases, typically mature teratoma. NMDAR-AIE is rarely associated with immature ovarian teratomas. Here, we describe three cases of NMDAR-AIE associated with immature ovarian teratomas. We review diagnosis and management of immature ovarian teratomas in NMDAR-AIE as a collaboration between gynecology and neurology, with multi-disciplinary recommendations provided regarding workup and management.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"412 ","pages":"Article 578850"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145849394","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":"Mitochondrial dysregulation as a central mechanism in autism spectrum disorder pathogenesis","authors":"Xiaoli Liao ,&nbsp;Jingqi Shao ,&nbsp;Zhihui Chen","doi":"10.1016/j.jneuroim.2025.578851","DOIUrl":"10.1016/j.jneuroim.2025.578851","url":null,"abstract":"<div><div>Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder influenced by both genetic predispositions and environmental insults. However, the precise molecular mechanisms linking prenatal environmental perturbations to neurodevelopmental impairments remain poorly defined. This study investigates the role of mitochondrial dysfunction and metabolic disturbances in ASD pathogenesis using various preclinical models, including the maternal immune activation (MIA) and ASD high-risk gene knockout models. We performed transcriptomic profiling on mouse brain tissues to identify differentially expressed genes (DEGs) associated with mitochondrial and metabolic pathways. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), revealed significant disruptions in pathways such as oxidative phosphorylation, tricarboxylic acid, and energy metabolism. These findings point to mitochondrial dysfunction as a central mechanism contributing to metabolic imbalances in ASD. Comparative analysis with publicly available RNA-seq datasets from PTEN knockout model revealed both shared and unique metabolic signatures. Single-cell RNA-seq data from the MIA model further identified cell-type-specific metabolic alterations in distinct neuronal and glial populations. Additionally, analysis of the Human Fetal Single-Cell Atlas highlighted the relevance of these metabolic pathways in human brain development. Collectively, these results emphasize mitochondrial metabolism as a potential therapeutic target for ASD, offering insights into the molecular basis of this disorder.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"412 ","pages":"Article 578851"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145912017","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":"Efficacy and tolerability of metformin as an adjuvant therapy in patients with relapse-remitting multiple sclerosis receiving interferon Beta 1a: A randomized pilot trial","authors":"Mohamed Y. Abdelgaied ,&nbsp;Omar Abdelgawad ,&nbsp;Mohamed Hamed Rashad ,&nbsp;Mohamed H. Solayman ,&nbsp;Hend M. El-Tayebi","doi":"10.1016/j.jneuroim.2025.578852","DOIUrl":"10.1016/j.jneuroim.2025.578852","url":null,"abstract":"<div><h3>Background</h3><div>Neurodegeneration and inflammation can accelerate the demyelination process in multiple sclerosis (MS). We aimed to investigate the efficacy and tolerability of metformin as an add-on treatment to interferon Beta 1a (IFNβ-1a) in Egyptian patients with relapsing-remitting multiple sclerosis (RRMS).</div></div><div><h3>Method</h3><div>Thirty RRMS patients were divided into two groups: the experimental arm receiving IFNβ-1a plus 2 g of metformin once daily and the control arm receiving IFNβ-1a alone. Tolerance to metformin was measured for the intervention group. Following 6 months period, serum neurofilament light chain (sNFL) and nuclear factor Kappa B (NF-κB), T2 lesions in magnetic resonance imaging (MRI), and expanded disability status scale (EDSS) were measured.</div></div><div><h3>Results</h3><div>There were no statistically significant differences between the two groups in the change in the median (interquartile range) of the blood biomarkers (sNFL; −32.8 (21) vs −32.8 (13.4), <em>p</em> = 0.99) and NF-κB; −64.9 (35.1) vs −61.6 (35.7), <em>p</em> = 0.8, respectively). In clinical outcomes, there was no statistically significant in the mean (standard deviation) change of EDSS (0 vs 0, <em>p</em> = 1)<strong>.</strong> For MRI results, 11 patients had a stationary and regressive course 1 patient had a progressive course in the metformin group vs 6 patients had a stationary and regressive course and 2 had a progressive course in the control group, <em>p</em> = 0.23. All outcomes were measured after 6-month follow-ups. The most common side effects of metformin were diarrhea and abdominal pain without incidence of lactic acidosis.</div></div><div><h3>Conclusion</h3><div>Receiving metformin as an add-on therapy to IFNβ-1a did not result in a significant improvement in neurodegeneration and inflammation blood biomarkers and clinical outcomes. A high dose of metformin (2 g/day) is safe and well tolerated in patients with MS. Additional studies involving larger populations are necessary to confirm or disprove these findings.</div></div><div><h3>Trial registration</h3><div><span><span>ClinicalTrials.gov</span><svg><path></path></svg></span> ID: <span><span>NCT06812585</span><svg><path></path></svg></span></div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"412 ","pages":"Article 578852"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145882029","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":"A case of Homer-3 IgG cerebellar ataxia & literature review of 15 reported cases","authors":"Diana Anissian ,&nbsp;Divyanshu Dubey ,&nbsp;Nisa Vorasoot ,&nbsp;Ramona Miske ,&nbsp;Anastasia Zekeridou ,&nbsp;Andrew McKeon","doi":"10.1016/j.jneuroim.2025.578846","DOIUrl":"10.1016/j.jneuroim.2025.578846","url":null,"abstract":"<div><div>Homer-3-IgG autoimmunity is a rare diagnosis typically presenting with subacute cerebellar ataxia. Here, we report a patient presenting insidiously with cerebellar ataxia and mild cognitive impairment, referred to the Mayo Clinic for a second opinion of her initial diagnosis of parkinsonism. Considering autoimmune cerebellar ataxia as the correct diagnosis, the patient's cerebrospinal fluid (CSF) and serum samples were sent for Movement Disorders Autoimmune/Paraneoplastic Evaluation neural antibody testing. Murine tissue-based indirect immunofluorescence assay of serum and CSF revealed a unique cerebellar molecular layer-predominant ‘medusa head’ staining pattern. Protein microarray disclosed Homer-3 as high ranking hits. Serological diagnosis was confirmed by Homer-3-specific line blot assay. The patient was treated with a 12-week regimen of intravenous methylprednisolone. She had limited improvement, though at 6-month follow-up she had not progressed further off treatment. This patient is the third detected case with Homer-3-IgG in the Neuroimmunology laboratory of the Mayo Clinic, and the only one clinically evaluated at Mayo Clinic. Histories for the two other cases were unavailable. This case adds to the limited number of reports on Homer-3-IgG autoimmunity, with our literature review identifying 15 other cases reported to date. Neurological presentations include cerebellar ataxia (15/16), cognitive impairment (4/16), REM sleep behavior disorder (2/16), seizures (2/16), myeloradiculopathy (1/16), radiculoneuropathy (1/16), and psychosis (1/16). The most common treatment used was corticosteroids (15/16), followed by IVIg (7/16), mycophenolate mofetil (MMF) (4/16), plasma exchange (3/16), and rituximab (1/16). Reported outcomes have varied, with partial improvement being most common (7/15).</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"412 ","pages":"Article 578846"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145839091","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":"Pilot analysis of Chitinase-3-like protein 1 and soluble Syndecan-1 CSF levels as potential biomarkers in relapsing-remitting multiple sclerosis","authors":"Firdevs Uluc ,&nbsp;Dursun Ceylan ,&nbsp;Sule Aydin Turkoglu","doi":"10.1016/j.jneuroim.2025.578836","DOIUrl":"10.1016/j.jneuroim.2025.578836","url":null,"abstract":"<div><h3>Background</h3><div>Chitinase-3-like protein 1 (CHI3L1), secreted by immune cells, plays a key role in modulating immune responses. Syndecan-1 (SDC-1), a cell surface heparan sulfate proteoglycan, is involved in the regulation of inflammation. This study aimed to evaluate whether CHI3L1 and soluble SDC-1 (sSDC-1) act as potential diagnostic targets in patients with relapsing-remitting multiple sclerosis (RRMS).</div></div><div><h3>Methods</h3><div>sSDC-1 and CHI3L1 levels were quantified using enzyme-linked immunosorbent assay (ELISA) in cerebrospinal fluid (CSF) samples collected from a cohort of 39 newly diagnosed patients with relapsing-remitting multiple sclerosis (RRMS) and 32 disease controls diagnosed with idiopathic intracranial hypertension (IIH).</div></div><div><h3>Results</h3><div>No significant difference was observed in CSF sSDC-1 levels between the RRMS and IIH groups. However, CSF CHI3L1 levels were significantly lower in patients with RRMS compared to those with IIH.</div></div><div><h3>Conclusion</h3><div>The present findings do not provide clear evidence supporting a diagnostic role for CSF levels of sSDC-1 or CHI3L1 in MS.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578836"},"PeriodicalIF":2.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145734292","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":"Comparison of SIMOA and VEUS technologies for serum glial fibrillary acidic protein measurement","authors":"Radovan Bunganic ,&nbsp;Kamila Zondra Revendova ,&nbsp;Pavel Hradilek ,&nbsp;Pavlina Kusnierova","doi":"10.1016/j.jneuroim.2025.578825","DOIUrl":"10.1016/j.jneuroim.2025.578825","url":null,"abstract":"<div><h3>Introduction</h3><div>Serum glial fibrillary acidic protein (sGFAP) is increasingly studied as a biomarker of astroglial injury, but comparative data between ultra-sensitive analytical platforms are limited. This study evaluated the agreement between the newly developed VEUS technology and the established single-molecule array (SIMOA) method.</div></div><div><h3>Methods</h3><div>A single-centre retrospective analysis was conducted at the Department of Neurology, University Hospital Ostrava. Patients ≥18 years with relapsing-remitting multiple sclerosis, non-inflammatory neurological disorders, or symptomatic controls were included. sGFAP levels were measured using the SIMOA GFAP Advantage PLUS Kit (Quanterix) and the Duplex RUO Kit (GFAP/UCH-L1) (VEUDx, EZDiatech). Method comparison included Spearman correlation, Passing–Bablok regression, and Bland–Altman analysis. Outliers were removed using Tukey's IQR rule.</div></div><div><h3>Results</h3><div>Fifty-six patients (78.6 % women) were included. SIMOA reported markedly higher sGFAP concentrations (median 110.5 ng/L, IQR 83.2–176) compared with VEUS (median 6.13 ng/L, IQR 3.88–6.87). No significant correlation was observed between platforms (<em>r</em> = 0.02, <em>p</em> = 0.89). Passing–Bablok regression demonstrated a near-zero slope, indicating absent linear association. Bland–Altman analysis showed proportional bias, with VEUS measuring on average 21 % of SIMOA values and increasing divergence at higher concentrations.</div></div><div><h3>Conclusion</h3><div>These results do not support substituting sGFAP measurements between VEUS and SIMOA assays.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578825"},"PeriodicalIF":2.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668830","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":"Neurobiotech innovative strategies targeting Alzheimer's disease through therapeutic micro and macroalgae potentials","authors":"Merna Wagdy ,&nbsp;Abeer A. Ibrahim ,&nbsp;Alaa M. Yahia,&nbsp;Rola M. Maher,&nbsp;Afaf Hany Abo-Elwafa,&nbsp;Alyaa Salah,&nbsp;Yasmin M. Heikal","doi":"10.1016/j.jneuroim.2025.578821","DOIUrl":"10.1016/j.jneuroim.2025.578821","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a progressive neurodegenerative disorder identified by cognitive decline, memory loss, and behavioral changes, affecting approximately 50 million people worldwide. Genetic predisposition, environmental variables, and aging all play a role in the development of AD. Current therapeutic approaches primarily focus on alleviating symptoms through drugs such as donepezil and memantine. However, these treatments offer limited efficacy and may be accompanied by adverse effects. In contrast, natural therapies derived from algae present a promising alternative. Microalgae, including Chlorella and Spirulina, and macroalgae such as <em>Fucus vesiculosus</em>, <em>Ecklonia cava</em>, Sargassum, <em>Laminaria japonica</em>, and Fucus species, are rich in bioactive molecules having antioxidant and anti-inflammatory characteristics. These substances demonstrated potential in addressing the pathological features of AD, such as oxidative stress and neuroinflammation. Furthermore, advances in biotechnological tools like CRISPR-Cas9 gene editing are poised to enhance the efficacy of these natural therapies by targeting and modifying disease-associated genes. This review aims to bridge the fields of neurobiotechnology and marine bioresources by examining the synergistic potential of algal compounds and gene-editing strategies in combating Alzheimer's disease. Algal-derived compounds are utilized in pharmaceuticals, nutraceuticals, and dietary supplements, and may offer neuroprotective benefits that could aid in the prevention or treatment of AD.By integrating insights from molecular biology, pharmacology, and genomics, we seek to illuminate a novel, multidisciplinary framework for future therapeutic innovation.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"411 ","pages":"Article 578821"},"PeriodicalIF":2.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668862","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}