Journal of Neurochemistry最新文献

{"title":"Exploring the Gut and Oral Microbiomes in Psychoactive Substance Use: A Scoping Review of Clinical Studies","authors":"Artūras Barkus,&nbsp;Vaida Baltrūnienė,&nbsp;Lina Barkienė,&nbsp;Justė Baušienė,&nbsp;Tomas Baltrūnas,&nbsp;Marius Brazys,&nbsp;Kornelija Rauduvytė,&nbsp;Paulina Kazlauskaitė,&nbsp;Augustinas Baušys","doi":"10.1111/jnc.70165","DOIUrl":"https://doi.org/10.1111/jnc.70165","url":null,"abstract":"<p>Substance use disorders (SUDs) constitute a significant global health challenge, and emerging evidence suggests that the gut and oral microbiomes may play significant roles in addiction pathophysiology, yet the human clinical literature remains fragmented. This scoping review systematically synthesizes evidence from 75 clinical studies investigating alterations in gut and oral microbiomes associated with alcohol, stimulant, cannabis, and opioid use. Across studies, beta-diversity analyses frequently reveal clear differences between substance users and controls, indicating distinct community structures. Findings on alpha diversity and specific taxonomic shifts vary by substance. Commonly observed changes included declines in beneficial short-chain fatty acid-producing taxa, alongside expansions of opportunistic or proinflammatory microorganisms. However, substantial methodological heterogeneity, including variations in study design, population characteristics, and analytical methods, complicates direct comparisons and definitive conclusions. Limited longitudinal evidence indicates partial microbiome recovery after extended abstinence, although full restoration remains uncertain. Further longitudinal research with standardized methods is needed to clarify these findings and inform potential microbiome-targeted therapies for SUDs.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70165","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144695858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ergothioneine Treatment Ameliorates the Pathological Phenotypes of Parkinson's Disease Models","authors":"Teddy J. W. Tng,&nbsp;Damien M. K. Leow,&nbsp;Geraldine Goh,&nbsp;Ziyin Wang,&nbsp;Yanmei Liu,&nbsp;Richard M. Y. Tang,&nbsp;Kate C. L. Lai,&nbsp;Adeline H. Basil,&nbsp;Huey Ching Choong,&nbsp;Wilson W. B. Goh,&nbsp;Irwin K. Cheah,&nbsp;Wei-Yi Ong,&nbsp;Barry Halliwell,&nbsp;Kah-Leong Lim","doi":"10.1111/jnc.70168","DOIUrl":"https://doi.org/10.1111/jnc.70168","url":null,"abstract":"<p>Ergothioneine (ET) is a naturally occurring thiol/thione that possesses several cytoprotective properties. Multiple studies suggest a potential neuroprotective role for ET. Here, we show in various Parkinson's disease (PD) models that ET is indeed neuroprotective. Firstly, using <i>Drosophila</i> genetic PD models, we demonstrated that ET treatment ameliorates the pathological phenotypes of <i>parkin</i> and <i>LRRK2</i> PD mutant flies. This includes an improvement in their climbing score and the preservation of their dopaminergic neuronal number and mitochondrial integrity. Similarly, we observed the rescue of PD phenotypes by ET in mice treated with the Parkinsonian neurotoxin 6-OHDA. This protective effect of ET is abolished in mice lacking OCTN1. Finally, we found that ET protects human LRRK2-G2019S patient-derived dopaminergic neurons from rotenone-induced neurotoxicity; the action of ET is again OCTN1-dependent. Collectively, our results strongly support a neuroprotective role for ET in PD and suggest that ET may be useful in the prevention and/or treatment of PD.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70168","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144681463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-Specific Distribution of Glycine Transporter 2 in the Central Nervous System of Adult GlyT2-iCre-tdTomato Mouse Brain","authors":"Zhenhua Jiang,&nbsp;Chenchen Huang,&nbsp;You Li,&nbsp;Jiajia Wang,&nbsp;Jing Qi,&nbsp;Jianshuai Zhao,&nbsp;Wenqiang Zuo,&nbsp;Peizheng Liu,&nbsp;Xiao Zhang,&nbsp;Xiaolan He,&nbsp;Minghui Wang,&nbsp;Nan Gu,&nbsp;Wugang Hou,&nbsp;Yan Lu,&nbsp;Qun Wang","doi":"10.1111/jnc.70135","DOIUrl":"https://doi.org/10.1111/jnc.70135","url":null,"abstract":"<div>\u0000 \u0000 <p>Glycine critically regulates locomotor and sensory processing, with its presynaptic glycine transporter 2 (GlyT2) serving as key therapeutic targets for modulating glycinergic neurotransmission. While GlyT2 inhibitors hold clinical promise, the specialization of spatially distributed GlyT2 neuronal populations across the brain remains incomplete. Here, we crossed GlyT2-iCre with Ai9 to generate GlyT2-iCre-tdTomato mice, enabling anatomical mapping and functional interrogation of GlyT2 circuits. Here, we generated GlyT2-iCre-tdTomato mice through crossbreeding GlyT2-iCre and Ai9 lines, enabling anatomical mapping and functional interrogation of GlyT2 circuits. Systematic quantification revealed sex- and region-specific neuronal distributions: non-estrus females exhibited significantly higher GlyT2-tdTomato neuron densities than males in 12 brain regions spanning thalamus (anterodorsal, anteroventral dorsomedial thalamic nucleus), midbrain (ventral periaqueductal gray, precommissural nucleus of the lateral lemniscus, superior and lateral parabrachial nucleus), and hindbrain (pontine nucleus, reticular oralis, reticulotegmental nucleus of the pons, rostromedial tegmental nucleus, solitary nucleus, interpolar part of spinal trigeminal nucleus), whereas males surpassed females in ventral posteromedial nuclei and lateral cerebellar regions. No sex differences were detected in 17 regions, including thalamic nuclei (anteromedial and ventral medial nucleus), posterior hypothalamus, substantia nigra, ventral nucleus of the lateral lemniscus, the nucleus of the central acoustic tract, ventral periolivary nucleus, paralemniscal nucleus, cerebellum, lateral periaqueductal gray, superior colliculus, inferior colliculus, medial parabrachial nucleus, and isthmic reticular formation. Spatial alignment with <i>GlyT2mRNA</i> data from the GlyT2-ISH atlas validated model specificity, establishing this resource as a foundation for investigating circuit-specific GlyT2 functions. These findings not only delineate organizational principles of glycinergic networks but also highlight sex as a critical variable in GlyT2 population architecture—a consideration essential for developing precision therapeutics targeting glycinergic dysfunction.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Embracing the Modern Biochemistry of Brain Metabolism","authors":"Juan P. Bolaños,&nbsp;Cristina M. Alberini,&nbsp;Angeles Almeida,&nbsp;L. Felipe Barros,&nbsp;Gilles Bonvento,&nbsp;Anne-Karine Bouzier-Sore,&nbsp;Ralf Dringen,&nbsp;Giles E. Hardingham,&nbsp;Johannes Hirrlinger,&nbsp;Pierre J. Magistretti,&nbsp;Giovanni Marsicano,&nbsp;Klaus-Armin Nave,&nbsp;Rosa C. Paolicelli,&nbsp;Luc Pellerin,&nbsp;Pierre-Yves Plaçais,&nbsp;Thomas Preat,&nbsp;Nathalie Rouach,&nbsp;Ivan Ruminot,&nbsp;Aiman S. Saab,&nbsp;Carmen Sandi,&nbsp;Stefanie Schirmeier,&nbsp;Avital Schurr,&nbsp;Jimena Sierralta,&nbsp;Maite Solas,&nbsp;Vanja Tepavcevic,&nbsp;Bruno Weber,&nbsp;Eduardo R. Zimmer","doi":"10.1111/jnc.70166","DOIUrl":"https://doi.org/10.1111/jnc.70166","url":null,"abstract":"<p>This editorial challenges the long-held neuron-centered view of brain metabolism, relying on ample evidence that it is a cooperative, multicellular process. Astrocytes, oligodendrocytes, and other glia play active roles providing lactate, antioxidant support, and substrate shuttles that fuel neuronal function and memory. Despite mounting data, some critics persist in refuting intercellular metabolic exchange, often guided more by entrenched creeds than concrete evidence, slowing constructive, hypothesis-driven discourse and delaying clinical and neuroprotective advances. The authors call for a rigorous research agenda: cell-type-specific manipulations, advanced biosensors, imaging and biomarkers, and integration with behavior and electrophysiology. They urge redirecting focus from outdated dogma to physiology-driven exploration of glia–neuron metabolic partnerships.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70166","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dissection of Neurochemical Pathways Across Complexity and Scale","authors":"Alice Abbondanza,&nbsp;Nawon Kim,&nbsp;Ricardo A. S. Lima-Filho,&nbsp;Azin Amin,&nbsp;Roberta G. Anversa,&nbsp;Felipe Borges Almeida,&nbsp;Pablo L. Cardozo,&nbsp;Giovanna Carello-Collar,&nbsp;Emma V. Carsana,&nbsp;Royhaan O. Folarin,&nbsp;Sara Guerreiro,&nbsp;Olayemi K. Ijomone,&nbsp;Sodiq K. Lawal,&nbsp;Isadora Matias,&nbsp;Smart I. Mbagwu,&nbsp;Sandra A. Niño,&nbsp;Bolanle F. Olabiyi,&nbsp;Sunday Y. Olatunji,&nbsp;Tosin A. Olasehinde,&nbsp;Waralee Ruankham,&nbsp;William N. Sanchez,&nbsp;Carina Soares-Cunha,&nbsp;Paula A. Soto,&nbsp;Jazmín Soto-Verdugo,&nbsp;Nathan R. Strogulski,&nbsp;Weronika Tomaszewska,&nbsp;Cármen Vieira,&nbsp;Adriano Chaves-Filho,&nbsp;Michael A. Cousin,&nbsp;Ago Rinken,&nbsp;Tyler J. Wenzel","doi":"10.1111/jnc.70160","DOIUrl":"https://doi.org/10.1111/jnc.70160","url":null,"abstract":"<p>The field of Neurochemistry spent decades trying to understand how the brain works, from nano to macroscale and across diverse species. Technological advancements over the years allowed researchers to better visualize and understand the cellular processes underpinning central nervous system (CNS) function. This review provides an overview of how novel models, and tools have allowed Neurochemistry researchers to investigate new and exciting research questions. We discuss the merits and demerits of different in vivo models (e.g., <i>Caenorhabditis elegans</i>, <i>Drosophila melanogaster</i>, <i>Ratus norvegicus</i>, and <i>Mus musculus</i>) as well as in vitro models (e.g., primary cells, induced pluripotent stem cells, and immortalized cells) to study Neurochemical events. We also discuss how these models can be paired with cutting-edge genetic manipulation (e.g., CRISPR-Cas9 and engineered viral vectors) and imaging techniques, such as super-resolution microscopy and new biosensors, to study cellular processes of the CNS. These technological advancements provide new insight into Neurochemical events in physiological and pathological contexts, paving the way for the development of new treatments (e.g., cell and gene therapies or small molecules) that aim to treat neurological disorders by reverting the CNS to its homeostatic state.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal Tryptophan Supplementation Alters Offspring Gut-Brain Axis and Behavior in a Sex-Specific Manner","authors":"Maria Carolina Fortunato,&nbsp;João Neves,&nbsp;Mariana Lapo Pais,&nbsp;Carla Fonseca,&nbsp;Daniela Silva,&nbsp;João Martins,&nbsp;Miguel Castelo-Branco,&nbsp;Ana Fortuna,&nbsp;Joana Gonçalves","doi":"10.1111/jnc.70161","DOIUrl":"https://doi.org/10.1111/jnc.70161","url":null,"abstract":"<div>\u0000 \u0000 <p>The maternal diet is a key determinant of offspring neurodevelopment, influencing gut microbiota composition and the gut-brain axis. These interactions are critical in shaping sex-specific vulnerabilities to neuropsychiatric disorders. Tryptophan, an essential amino acid and precursor to serotonin, plays a pivotal role in neurodevelopment and immune function. However, the impact of maternal tryptophan supplementation on healthy offspring's neurochemical and behavioral outcomes remains unclear. This study investigated the effects of a tryptophan-enriched maternal diet on offspring gut microbiota, metabolism, neurochemical pathways, and behavior. We analyzed microbial composition, metabolic activity, brain, and plasma levels of tryptophan and serotonin, and behavioral outcomes in male and female mice offspring. Maternal tryptophan supplementation led to sex-specific changes. Female offspring exhibited disrupted microbiota diversity, reduced brain tryptophan and serotonin levels, and heightened anxiety-like behaviors. In contrast, male offspring displayed increased metabolic activity, elevated brain tryptophan levels, and repetitive behaviors. These findings suggest that maternal tryptophan supplementation influences offspring neurodevelopment and behavior by modulating gut-brain axis components in a sex-dependent manner. This work underscores the importance of further research into prenatal dietary interventions targeting gut microbiota and neurochemical pathways to support healthy neurodevelopment and potentially inform sex-specific preventive strategies. These findings contribute to a growing understanding of how maternal nutrition influences offspring neurodevelopment and may guide the development of preventive strategies to improve long-term mental health outcomes..\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144657624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Status and Prospects of Glioblastoma Multiforme Treatments","authors":"Xue Yang,&nbsp;Shibing Wang,&nbsp;Vedrana Montana,&nbsp;Xiangmin Tong,&nbsp;Vladimir Parpura","doi":"10.1111/jnc.70158","DOIUrl":"https://doi.org/10.1111/jnc.70158","url":null,"abstract":"<p>Glioblastoma multiforme (GBM) is the most aggressive and common primary brain cancer in adults. Its standard-of-care therapy encompasses surgical resection, radiotherapy, and chemotherapy. Although this combination therapy somewhat extends patient survival, its efficacy remains limited, and the recurrence rate remains high. In recent years, novel therapeutic approaches for the treatment of GBM have emerged: (i) tumor-treating fields delivering nonionizing low-intensity alternating electric fields to disrupt mitosis; (ii) molecular targeted therapies that inhibit specific gene mutations or signaling pathways; (iii) immunotherapy that activates the patient's own immune system to fight this cancer; (iv) proton therapy, which, with its precise radiation dose distribution, minimizes damage to the normal brain parenchyma surrounding the GBM; (v) oncolytic virus therapy to selectively infect and lyse GBM cells; (vi) the use of nanoparticle carriers for targeted drug delivery to increase therapeutic efficacy and reduce side effects; (vii) phototherapy; and (viii) sonodynamic therapy. The purpose of this narrative is to review both standard-of-care and novel contemporary approaches to this devastating cancer. In the future, with further advancements in multiomics technologies, artificial intelligence, and novel biomaterials, GBM treatment should move toward more personalized, precise, and comprehensive approaches, offering patients more effective treatment options.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144657625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of pTau181 by Glypican-1-Derived Heparan Sulfate in Human Neural Progenitor Cells and ApoE4-Expressing Induced Neurons","authors":"Fang Cheng,&nbsp;Lars-Åke Fransson,&nbsp;Katrin Mani","doi":"10.1111/jnc.70162","DOIUrl":"https://doi.org/10.1111/jnc.70162","url":null,"abstract":"<p>In Alzheimer's disease (AD) there is accumulation of amyloid-β (Aβ) and hyperphosphorylated tau (pTau) in the brain. Aβ activates kinases that phosphorylate tau. Increased pTau181 is a signal for hyperphosphorylation of tau. The generation of Aβ from amyloid precursor protein (APP) and the release of heparan sulfate (HS) from the proteoglycan glypican-1 (GPC1) are interconnected. Release of HS is APP-, ascorbate-, copper-, and NO-dependent. HS-Aβ interactions may regulate tau phosphorylation in human neural stem cells (NSC). The most influential risk factor for sporadic AD is the presence of the ε4 allele of apolipoprotein E (ApoE). Here, we have further explored the interplay between GPC1-derived HS and pTau181 formation in human neural progenitor cells (NPC) and induced neurons (iN) obtained by reprogramming of human fibroblasts from ApoE3- and ApoE4-carriers. HS release from GPC1 was either suppressed or stimulated, and effects on pTau181 were monitored by immunofluorescence microscopy and quantified by intensity measurements as well as by enzyme-linked immunosorbent assay (ELISA) technique. Stimulation of HS release decreased pTau181 in NSC but was without effect in NPC, where tau was mostly in the nuclei. However, suppression of HS release in NPC increased pTau181. Stimulation of HS release decreased pTau181 in ApoE4/4-iN but not in ApoE3/3-iN. A high intake of vitamin C may be of prophylactic value in ApoE4-positive individuals.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70162","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “The Serine/Threonine Kinase NDR2 Regulates Integrin Signaling, Synapse Formation, and Synaptic Plasticity in the Hippocampus”","authors":"","doi":"10.1111/jnc.70149","DOIUrl":"https://doi.org/10.1111/jnc.70149","url":null,"abstract":"<p>del Ángel, M., Tsutiya, A., Hayani, H., Madencioglu, D., Kul, E., Caliskan, G., Demiray, Y.E., Dityatev, A., and Stork, O. (2025). The Serine/Threonine Kinase NDR2 Regulates Integrin Signaling, Synapse Formation, and Synaptic Plasticity in the Hippocampus. <i>Journal of Neurochemistry</i>, 169: e70094. https://doi.org/10.1111/jnc.70094.</p><p>In the paper by del Ángel et al. (2025), the first author's name appeared incorrectly. The author's correct name is Miguel del Ángel.</p><p>The original paper has now been corrected.</p><p>We apologize for this error.</p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70149","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144624813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Role of Microglial Cells in the Gut–Brain Axis Communication: A Systematic Review","authors":"Nadia Suyin Ortiz-Samur,&nbsp;Akshay Kumar Vijaya,&nbsp;Aurelijus Burokas,&nbsp;Virginia Mela","doi":"10.1111/jnc.70154","DOIUrl":"https://doi.org/10.1111/jnc.70154","url":null,"abstract":"<p>The gut–brain axis (GBA) is a bidirectional communication system between the gastrointestinal tract and the CNS, playing a key role in neurological function, immune response, and metabolism. Microglia, the resident immune cells in the brain, are crucial regulators of neuroinflammation and synaptic plasticity. Recent studies indicate that the gut microbiota modulates microglial activity through metabolic and immune pathways, with implications for neurodegenerative, neurodevelopmental, and psychiatric disorders. However, the mechanisms underlying microbiota–microglia interactions remain unclear. Following a systematic screening of 4481 studies, 20 preclinical studies met the inclusion criteria and were reviewed in depth to assess microbiota–microglia interactions. These studies were found by searching in PubMed, Science Direct, and Google Scholar. The findings synthesize results from 20 carefully selected studies examining the impact of gut microbiota on microglial function. Experimental models, including fecal microbiota transplantation, dietary interventions, and bacterial supplementation, were analyzed. Microglial activity was assessed through immunohistochemistry, gene expression profiling, and functional assays. Most studies suggest that gut dysbiosis promotes microglial overactivation and neuroinflammation through pathways involving microbial-derived short-chain fatty acids (SCFAs), bile acids, and neuroimmune signaling cascades such as TLR4/NF-κB and the NLRP3 inflammasomes, whereas microbiota-targeted interventions reduce inflammation and support cognitive function. Despite these promising findings, inconsistencies in study methodologies and microbiota analyses limit comparability and clinical translation. This review offers a unique synthesis of studies specifically linking gut microbiota alterations to microglial states, neuroinflammatory signatures, and cognitive outcomes across diverse experimental models. It highlights the therapeutic potential of microbiota-based strategies for modulating microglial function and mitigating neuroinflammatory diseases.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 7","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70154","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144624831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}