Pub Date : 2026-02-04DOI: 10.1186/s12974-025-03677-z
Nan Zhang, Wei-Ming Su, Ting Chen, Qin Zhang, Bei Cao, Yi Wang, Yong-Ping Chen
{"title":"From pathogenesis to therapy: the emerging role of regulatory T cells in amyotrophic lateral sclerosis.","authors":"Nan Zhang, Wei-Ming Su, Ting Chen, Qin Zhang, Bei Cao, Yi Wang, Yong-Ping Chen","doi":"10.1186/s12974-025-03677-z","DOIUrl":"10.1186/s12974-025-03677-z","url":null,"abstract":"","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"23 1","pages":"50"},"PeriodicalIF":10.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12870331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-03DOI: 10.1186/s12974-026-03718-1
Jayden A O'Brien, Frederick A Collin, Ava C Mason, Rebecca V Robertson, Sachin Shetty, Iain S McGregor, Luke A Henderson, Paul J Austin
Spinal cord injury is a severe neurological condition associated with an increased risk of infection, an elevated mortality rate, and often results in chronic neuropathic pain. The peripheral immune changes in the chronic phase of spinal cord injury are largely unknown, as is their capacity to facilitate neuropathic pain. The current study used a high-dimensional single-cell analysis of peripheral blood to evaluate major immune populations and functional markers in individuals with chronic spinal injury. Spinal cord injury was associated with a shift towards classical monocytes and an increase in granulocytic myeloid-derived suppressor cells. There were also reductions in NK cells and B cells, as well as impairments to memory T cell functioning. The elevation of classical monocytes and decrease in NK cells were more pronounced in injured individuals with neuropathic pain, a high spinal level of lesion, and a moderate, but not severe injury. These findings highlight the cell-specific systemic immune dysfunction in chronic spinal cord injury and how more severe clinical subgroups are largely associated with greater immune impairment. Therefore, targeting immune dysfunction may lead to an improvement in symptom severity, whilst biomarkers of immune dysfunction may be useful in predicting the clinical trajectory.
{"title":"Peripheral immunosuppressive and immunostimulatory signatures of severity and pain in spinal cord injury.","authors":"Jayden A O'Brien, Frederick A Collin, Ava C Mason, Rebecca V Robertson, Sachin Shetty, Iain S McGregor, Luke A Henderson, Paul J Austin","doi":"10.1186/s12974-026-03718-1","DOIUrl":"https://doi.org/10.1186/s12974-026-03718-1","url":null,"abstract":"<p><p>Spinal cord injury is a severe neurological condition associated with an increased risk of infection, an elevated mortality rate, and often results in chronic neuropathic pain. The peripheral immune changes in the chronic phase of spinal cord injury are largely unknown, as is their capacity to facilitate neuropathic pain. The current study used a high-dimensional single-cell analysis of peripheral blood to evaluate major immune populations and functional markers in individuals with chronic spinal injury. Spinal cord injury was associated with a shift towards classical monocytes and an increase in granulocytic myeloid-derived suppressor cells. There were also reductions in NK cells and B cells, as well as impairments to memory T cell functioning. The elevation of classical monocytes and decrease in NK cells were more pronounced in injured individuals with neuropathic pain, a high spinal level of lesion, and a moderate, but not severe injury. These findings highlight the cell-specific systemic immune dysfunction in chronic spinal cord injury and how more severe clinical subgroups are largely associated with greater immune impairment. Therefore, targeting immune dysfunction may lead to an improvement in symptom severity, whilst biomarkers of immune dysfunction may be useful in predicting the clinical trajectory.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-02DOI: 10.1186/s12974-026-03700-x
Marjo Nylund, Jussi Lehto, Markus Matilainen, Johan Rajander, Saara Wahlroos, Marcus Sucksdorff, Tanja Kuhlmann, Laura Airas
{"title":"Correction: Longitudinal accumulation of glial activation measured by TSPO-PET predicts later brain atrophy in multiple sclerosis.","authors":"Marjo Nylund, Jussi Lehto, Markus Matilainen, Johan Rajander, Saara Wahlroos, Marcus Sucksdorff, Tanja Kuhlmann, Laura Airas","doi":"10.1186/s12974-026-03700-x","DOIUrl":"10.1186/s12974-026-03700-x","url":null,"abstract":"","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"23 1","pages":"46"},"PeriodicalIF":10.1,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12862898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146105944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-31DOI: 10.1186/s12974-026-03712-7
Pablo Scharf, Silvana Sandri, Pâmela Pacassa Borges, Tiago Francisco da Silva, Laura Caroline de Faria, Luana Filippi Xavier, Ana Victoria Dos Santos Helfstein, Augusto César Penalva de Oliveira, Guilherme Sciacia do Olival, Jean Pierre Peron Schatzmann, Sandra Helena Poliselli Farsky
{"title":"Heated tobacco and cigarette smoke modulate CD4 + T cell activation and neuroinflammation in a context-dependent manner.","authors":"Pablo Scharf, Silvana Sandri, Pâmela Pacassa Borges, Tiago Francisco da Silva, Laura Caroline de Faria, Luana Filippi Xavier, Ana Victoria Dos Santos Helfstein, Augusto César Penalva de Oliveira, Guilherme Sciacia do Olival, Jean Pierre Peron Schatzmann, Sandra Helena Poliselli Farsky","doi":"10.1186/s12974-026-03712-7","DOIUrl":"https://doi.org/10.1186/s12974-026-03712-7","url":null,"abstract":"","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-31DOI: 10.1186/s12974-026-03716-3
Maria Luque, Magdalena Matic, Antonio Heras-Garvin, Jesus Amo-Aparicio, Kelvin C Luk, Michaela Tanja Haindl, Michael Khalil, Damaris B Skouras, Charles A Dinarello, Nadia Stefanova
{"title":"Clinically advanced NLRP3 inhibitor modulates microglial transcriptome and alleviates α-synuclein-induced progression of parkinsonism.","authors":"Maria Luque, Magdalena Matic, Antonio Heras-Garvin, Jesus Amo-Aparicio, Kelvin C Luk, Michaela Tanja Haindl, Michael Khalil, Damaris B Skouras, Charles A Dinarello, Nadia Stefanova","doi":"10.1186/s12974-026-03716-3","DOIUrl":"https://doi.org/10.1186/s12974-026-03716-3","url":null,"abstract":"","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-29DOI: 10.1186/s12974-025-03664-4
Hyun Jung Kwon, Ji Hyeon Ahn, Moo-Ho Won, Dae Won Kim
Chronic periodontitis is increasingly recognized as a potential upstream contributor to neurodegenerative processes through sustained systemic inflammation, microbial dysbiosis, and blood-brain barrier (BBB) alterations. This review synthesizes human and experimental evidence linking periodontal pathogens-including but not limited to Porphyromonas gingivalis as well as broader dysbiotic consortia such as Tannerella forsythia, Treponema denticola, and other keystone oral taxa-to neuroinflammatory cascades associated with cognitive decline. Mechanistic insights highlight the roles of glial activation, proinflammatory cytokines, and polymicrobial virulence-mediated neuronal stress in bridging oral and brain pathology, while age-related factors such as immunosenescence and microbiome imbalance amplify systemic vulnerability. Human biomarker and imaging studies support an association between chronic periodontal inflammation and neurovascular dysfunction, suggesting that oral disease may act as a persistent peripheral amplifier of central immune activation. Recent research has expanded into biomarker discovery and translational implementation, yet progress remains limited by population heterogeneity, methodological variability, and regulatory complexity. Promising interventions-including anti-inflammatory therapies, oral hygiene optimization, probiotic or dietary modulation, and molecular strategies such as polymicrobial-targeted approaches, gingipain inhibition, and microRNA-based modulation-are discussed within emerging multi-omics and precision-medicine frameworks. Although standardization and longitudinal validation are still required, integrative approaches combining inflammatory, microbial, and genetic profiling may enable individualized risk assessment and targeted prevention. As global populations age, addressing the oral-brain axis offers a practical and modifiable pathway to lessen the burden of neurodegenerative diseases and support healthier cognitive aging.
{"title":"Chronic periodontitis and systemic inflammation in the elderly: implications for neurodegeneration.","authors":"Hyun Jung Kwon, Ji Hyeon Ahn, Moo-Ho Won, Dae Won Kim","doi":"10.1186/s12974-025-03664-4","DOIUrl":"10.1186/s12974-025-03664-4","url":null,"abstract":"<p><p>Chronic periodontitis is increasingly recognized as a potential upstream contributor to neurodegenerative processes through sustained systemic inflammation, microbial dysbiosis, and blood-brain barrier (BBB) alterations. This review synthesizes human and experimental evidence linking periodontal pathogens-including but not limited to Porphyromonas gingivalis as well as broader dysbiotic consortia such as Tannerella forsythia, Treponema denticola, and other keystone oral taxa-to neuroinflammatory cascades associated with cognitive decline. Mechanistic insights highlight the roles of glial activation, proinflammatory cytokines, and polymicrobial virulence-mediated neuronal stress in bridging oral and brain pathology, while age-related factors such as immunosenescence and microbiome imbalance amplify systemic vulnerability. Human biomarker and imaging studies support an association between chronic periodontal inflammation and neurovascular dysfunction, suggesting that oral disease may act as a persistent peripheral amplifier of central immune activation. Recent research has expanded into biomarker discovery and translational implementation, yet progress remains limited by population heterogeneity, methodological variability, and regulatory complexity. Promising interventions-including anti-inflammatory therapies, oral hygiene optimization, probiotic or dietary modulation, and molecular strategies such as polymicrobial-targeted approaches, gingipain inhibition, and microRNA-based modulation-are discussed within emerging multi-omics and precision-medicine frameworks. Although standardization and longitudinal validation are still required, integrative approaches combining inflammatory, microbial, and genetic profiling may enable individualized risk assessment and targeted prevention. As global populations age, addressing the oral-brain axis offers a practical and modifiable pathway to lessen the burden of neurodegenerative diseases and support healthier cognitive aging.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"23 1","pages":"43"},"PeriodicalIF":10.1,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12853916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146086099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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