Inflammopharmacology最新文献

{"title":"Boswellic acids as an adjunct therapy in Parkinson's disease: a double-blind clinical trial investigating on its effects on motor symptoms and inflammatory markers.","authors":"Somayyeh Shateri, Seyyed Hossein Khatami, Sajad Ehtiati, Mohammad Reza Talebzadeh, Sadegh Nikakhtar, Monir Hassani Parvar, Seyedeh Ozra Hosseini, Gholamali Shahidi, Amir Hossein Habibi, Farzaneh Salmani, Fatemeh Namvarjah, Ali Riazi, Abbas Tafakhori, Saeed Karima","doi":"10.1007/s10787-025-01950-4","DOIUrl":"https://doi.org/10.1007/s10787-025-01950-4","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by postural instability, rigidity, bradykinesia, and resting tremors. Neuroinflammation has been implicated in PD pathogenesis, with inflammatory cytokines serving as potential biomarkers for disease progression and therapeutic monitoring. This study aimed to assess the effects of boswellic acids' supplementation (the main active component of Strowell®) on motor and cognitive function in PD patients, as well as its impact on inflammatory biomarkers.</p><p><strong>Methods: </strong>In a 6-month, randomized, double-blind, placebo-controlled clinical trial, 58 PD patients were assigned to receive either boswellic acids or a placebo. Clinical assessments included the Unified Parkinson's Disease Rating Scale (UPDRS) and the Montreal Cognitive Assessment (MoCA), with comparisons to baseline scores. Inflammatory biomarkers were measured at baseline and after 1 month.</p><p><strong>Results: </strong>After 6 months, UPDRS scores remained stable in the boswellic acids group but significantly worsened in the placebo group (p = 0.0008). MoCA scores showed a slight but non-significant improvement in the treatment group, while no improvement was observed in the placebo group. In addition, 1 month of boswellic acids' supplementation led to a significant reduction in plasma levels of pro-inflammatory cytokines, including IL-4, IL-1A, IL-12p70, INF-γ, IL-1β, TNF-α, IL-6, and PGE2.</p><p><strong>Conclusion: </strong>The findings suggest that boswellic acids' supplementation may help mitigate motor function decline in PD patients while exerting significant anti-inflammatory effects. These results support the potential role of boswellic acids as an adjunctive therapy for Parkinson's disease.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol supplementation improves functional performance in knee osteoarthritis by upregulating sirtuin 1: a randomized study.","authors":"Asima Karim, Haroon Ahmed Khan, Firdos Ahmad, Rizwan Qaisar","doi":"10.1007/s10787-025-01967-9","DOIUrl":"https://doi.org/10.1007/s10787-025-01967-9","url":null,"abstract":"<p><strong>Purpose: </strong>Osteoarthritis (OA) is a debilitating disease of joints. Currently, there are no optimal treatment options to cure OA.</p><p><strong>Objective: </strong>To determine whether resveratrol treatment can improve physical function in knee OA patients. Trial design This investigation employed a single center-based, double-blinded, randomized, placebo-regulated clinical trial structure.</p><p><strong>Methods: </strong>We led a 12-week clinical study involving 137 knee OA patients, aged 63-73. Participants were divided to form a placebo-taking group (n = 70) and an intervention group receiving 500 mg/day of resveratrol (n = 67). Data collection occurred at the start and after 12 weeks. Key study outcomes included: pain intensity (VAS), Oxford Knee Score (OKS), WOMAC index score, knee flexion range of motion (ROM), short physical performance battery (SPPB), handgrip strength (HGS), gait velocity, and levels of SIRT1, C-reactive protein (CRP), and 8-isoprostanes.</p><p><strong>Results: </strong>After accounting for dropouts, 122 patients were analyzed (placebo: n = 65, resveratrol: n = 57). Resveratrol treatment significantly reduced pain intensity and WOMAC scores, while increasing OKS scores, ROM, gait velocity, HGS, and overall SPPB performance (p < 0.05). In addition, OA patients on resveratrol showed higher plasma SIRT1 and lower 8-isoprostanes levels (p < 0.05). The correlation analysis demonstrated robust associations between changes in plasma SIRT1 and improvements in OKS scores (r² = 0.204, p = 0.0005), SPPB total (r² = 0.223, p = 0.0001), HGS (r² = 0.119, p = 0.008), and gait speed (r² = 0.138, p = 0.004).</p><p><strong>Conclusion: </strong>Overall, resveratrol supplementation enhances the physical capabilities of OA patients by increasing SIRT1 levels. Further research is warranted to more fully define resveratrol's impact on knee OA.</p><p><strong>Trial registration: </strong>This investigation was retrospectively registered on the Open Science Framework (OSF), ensuring transparency and accessibility of the study protocol and outcomes. Registration date (21st April 2025) and URL for protocol ( https://osf.io/registries/my-registrations ).</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium hydrogen sulfide restores H₂S-synthesizing and degrading enzymes to alleviate glial activation after traumatic brain injury in male mice.","authors":"Farheen Nasir, Priyanka Yadav, Thamil Mani Sivanandam","doi":"10.1007/s10787-025-01989-3","DOIUrl":"https://doi.org/10.1007/s10787-025-01989-3","url":null,"abstract":"<p><strong>Background and purpose: </strong>Traumatic brain injury (TBI) is a multifaceted pathological condition affecting people worldwide. Hydrogen sulfide (H₂S) is a newly identified gaseous mediator and is testified to be beneficial in various conditions of physiology and pathology. Following TBI, the regulation of H₂S is disrupted. Sodium hydrogen sulfide (NaHS) functions effectively as a source of H₂S. It functions against neuroinflammation in different neurological conditions, including injury, relieving the cascades of secondary injury processes. However, it has not been exploited to mitigate the adverse effects of TBI-induced glial activation, potentially by restoring the balance of H₂S synthesis and degradation.</p><p><strong>Experimental approach: </strong>We developed a weight-drop model of TBI to establish the effects of NaHS treatment. We validated our findings by behavioral tasks, estimated H₂S levels by fluorescent probe, quantitatively measured H₂S-synthesizing and degrading enzymes by immunoblotting, and analyzed the morphology of astrocytes and microglia by immunofluorescence.</p><p><strong>Key results: </strong>We found that NaHS treatment restored the H₂S levels by upregulating H₂S- synthesizing and downregulating H₂S-degrading enzymes post-TBI. It also mitigated TBI-induced neuroinflammation as depicted by the altered morphology of astrocytes and microglia. The reasons for such modifications were credited to the altered phosphorylation status of different kinases that facilitate the functions of many downstream signaling molecules in the S100β/RSK1 and RAS/RAF/MEK/ERK/NF-κB pathways.</p><p><strong>Conclusion and implications: </strong>The data gathered here suggest that NaHS could work well as a potential therapeutic agent against TBI-induced brain pathology, ameliorating astrocyte and microglia activation owing to alterations of proteins involved in H₂S synthesis and degradation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diallyl disulfide attenuates DSS-induced colonic fibrosis in mice by modulating gut microbiota and Nrf2 signaling.","authors":"Shuangshuang Hai, Yan Chen, Meiyan Zhang, Weixin Liu, Xiaohong Sun","doi":"10.1007/s10787-025-01984-8","DOIUrl":"https://doi.org/10.1007/s10787-025-01984-8","url":null,"abstract":"<p><strong>Background: </strong>The use of natural medicines as adjuvant therapies for fibrotic diseases has recently garnered significant attention. Diallyl disulfide (DADS), a bioactive sulfur compound from garlic, exhibits antioxidant, anti-inflammatory, and immunomodulatory effects, but its impact on colitis-associated intestinal fibrosis is unknown.</p><p><strong>Methods: </strong>We administered DADS (80 mg/kg orally) to mice with dextran sulfate sodium (DSS)-induced chronic colitis-associated intestinal fibrosis and assessed clinical parameters, histopathological, immunohistochemistry, 16S rDNA-based gut microbiota profiling, and Mendelian randomization analysis.</p><p><strong>Results: </strong>DADS treatment ameliorated weight loss, disease activity index (DAI), colon shortening and histological damage, and reduced inflammatory infiltration and collagen deposition. Mechanistically, DADS activated the Nrf2 antioxidant pathway, inhibited TGF-β1/Smad3 fibrogenic signaling, and favorably altered gut microbial diversity and composition.</p><p><strong>Conclusion: </strong>By engaging Nrf2, suppressing TGF-β1/Smad3 and modulating the gut microbiota, DADS attenuates colitis-associated intestinal fibrosis, highlight its potential as novel anti-fibrotic adjuvant.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-carnitine as a novel approach for pain and inflammation relief in rheumatoid arthritis.","authors":"Abdallah A Eldisouky, Sahar K Hegazy, Salwa Elmorsy Abd Elghany","doi":"10.1007/s10787-025-01956-y","DOIUrl":"https://doi.org/10.1007/s10787-025-01956-y","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by joint inflammation, largely mediated by pro-inflammatory cytokines. Considering the established involvement of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway and transforming growth factor-beta1 (TGF-β1) in RA, this research aimed to assess efficacy and safety of L-carnitine as an adjunct therapy targeting these pathways. Forty-six patients with active RA were randomly divided into two equal groups. Group1 (control group) received disease-modifying antirheumatic drugs (DMARDs), including methotrexate, leflunomide, and hydroxychloroquine. Group2 (L-carnitine group) received, DMARDs plus L-carnitine 500 mg twice daily for 12 weeks. A clinical evaluation was conducted, which included tender joint count (TJC), swollen joint count (SJC), pain intensity quantified via the visual analogue scale (VAS), and morning stiffness duration. Additionally, the Disease Activity Score in 28 joints (DAS28) and functional capability as measured by a modified health assessment questionnaire (MHAQ) were assessed. Laboratory evaluation included C-reactive protein (CRP), STAT3, and TGF-β1 measurement. All evaluations were executed both at baseline and following a 12-week treatment period. After 12 weeks, the L-carnitine group showed significant improvement in morning stiffness, VAS, TJC, CRP, DAS28, and MHAQ compared to baseline. While no significant within-group changes were observed in STAT3, TGF-β1 in the L-carnitine group, STAT3 levels increased significantly in the control group compared to baseline. In conclusion, L-carnitine in combination with DMARDs may enhance clinical outcomes in RA by mitigating systemic inflammation. Nevertheless, its impact on STAT3 and TGF-β1 remains unclear and warrants further research.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurodegeneration and aging: pathophysiology, diagnosis, and therapeutic targets.","authors":"Abhay Thakur, Rahul Sharma, Rohit Sharma, Anjana Devi","doi":"10.1007/s10787-025-01991-9","DOIUrl":"https://doi.org/10.1007/s10787-025-01991-9","url":null,"abstract":"<p><p>Aging is the greatest risk factor for AD, ALS, PD, FTD, and HD. Neurons in the brain experience many changes as people age, negatively affecting their structure and function. It examines the key processes behind brain aging, such as age-related death of cells, failure of the cells' powerhouses, oxidative stress, incorrect protein shapes, brain inflammation, difficulty in cleaning the brain, and deterioration of blood vessels, and shows their impact on neurodegeneration. With age, there are difficulties in brain-blood circulation, less synaptic change, and fewer new neurons, which make the disease even worse. Informed by human and animal trials, we see that mitochondria work less efficiently in aging brain cells, while oxidative damage to DNA increases doubly to triply. In addition, too much tau, amyloid-β, and α-synuclein building up is tied to declining mental abilities in the elderly. We further evaluate new tests that help with early detection and classification, for example, using biomarkers in cerebrospinal fluid (CSF), blood panels, detailed brain scans, and AI algorithms. It stresses that more aging-specific trials, better integration of multi-omics, and increased interest in research on the gut-brain axis are important. The communication between the aging of the body and the brain is also explained. This article covers the main cellular, molecular, and clinical issues linked to brain aging and highlights important future research areas needed to develop effective treatments for aging people.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical study evaluating the gastroprotective effect of carvedilol in patients with ischemic heart disease on aspirin therapy.","authors":"Sarah M Elkablawy, Aliaa E Shaban, Tarek M Mostafa","doi":"10.1007/s10787-025-01961-1","DOIUrl":"https://doi.org/10.1007/s10787-025-01961-1","url":null,"abstract":"<p><strong>Background and purpose: </strong>Despite its therapeutic benefits in ischemic heart disease (IHD) patients, using aspirin represents a significant risk of gastric ulcers. Therefore, this study aimed to inspect the gastroprotective potential of carvedilol in IHD patients undergoing aspirin treatment.</p><p><strong>Patients and methods: </strong>In this randomized, controlled parallel trial, 66 patients with IHD on aspirin therapy were assigned to group 1 (control, n = 33), received aspirin 150 mg plus captopril 12.5 mg twice daily and standard IHD medications, and group 2 (carvedilol group, n = 33), received aspirin 150 mg plus carvedilol 12.5 mg twice daily and standard IHD medications for three months. All patients were subjected to assessments for demographic data, anthropometric measurements, and biochemical measurements of the serum levels of malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), prostaglandin E2 (PGE2), and gastrin-17 (GAS-17). The researchers also evaluated the Structured Assessment of Gastrointestinal Symptoms (SAGIS) questionnaire and the Seattle Angina Questionnaire (SAQ-7) to assess changes in the quality of life (QOL).</p><p><strong>Results: </strong>Three months post-treatment and relative to the control group, the carvedilol group exhibited significantly reduced serum levels of MDA (P2 = 0.003), 4-HNE (P2 < 0.001), and GAS-17 (P2 = 0.015), which was associated with significantly higher serum levels of PGE2 (P2 < 0.001). Additionally, the carvedilol group showed a significantly higher SAQ-7 score (P2 = 0.033) and a significantly lower SAGIS questionnaire score (P2 = 0.04) than the control group.</p><p><strong>Conclusion: </strong>Carvedilol could represent a potential gastroprotective agent for patients with IHD on aspirin therapy secondary to its efficacy and safety.</p><p><strong>Clinicaltrial: </strong>gov ID: NCT05553717.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulating inflammation and oxidative stress in rheumatoid arthritis: a systematic review of nutraceutical interventions.","authors":"Camila Leiva-Castro, Ana M Múnera-Rodríguez, Gádor Torres-Joya, Francisca Palomares-Jerez, Soledad López-Enríquez","doi":"10.1007/s10787-025-01976-8","DOIUrl":"https://doi.org/10.1007/s10787-025-01976-8","url":null,"abstract":"<p><p>Rheumatoid arthritis is a chronic autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction. The gut microbiome has emerged as a key factor in the regulation of the immune system, and its dysbiosis has been implicated in the pathogenesis of rheumatoid arthritis. Nutraceuticals, including probiotics, omega-3 fatty acids, coenzyme Q10, vitamin D, and polyphenols, have shown potential in modulating the gut microbiota and inflammatory pathways. This review explores the interplay between nutraceuticals, gut microbiota, and immune function in rheumatoid arthritis, with attention to pharmacokinetics and safety. We discuss recent clinical evidence, elucidate molecular mechanisms of action, and highlight future research directions for integrating nutraceuticals into therapeutic strategies for rheumatoid arthritis.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential protective effect of Empagliflozin against Cisplatin-induced ovarian damage via upregulation of SIRT1/Nrf2 and amelioration ER Stress.","authors":"Magda E El-Sayad, Sally E Abu-Risha, Sarah S El-Sisi, Hanaa A Ibrahim","doi":"10.1007/s10787-025-01970-0","DOIUrl":"https://doi.org/10.1007/s10787-025-01970-0","url":null,"abstract":"<p><p>Cisplatin (Cis) is a chemotherapeutic agent used for several types of malignant tumors. Though, its use causes several adverse effects as ovarian toxicity through its effect on unbalancing antioxidant and oxidants causing oxidative stress and inflammation. The present study aimed to examine the potential protective effect of Empagliflozin (EMPA) on Cisplatin-induced ovarian damage. Forty-four adult female albino rats were divided into four groups: control group, EMPA group (EMPA 10 mg/kg/day, P.O) for 17 days, CIS group (CIS 7 mg/kg, I.P) on day 14, Cis + EMPA group, EMPA (10 mg/kg/day, P.O) for 17 days with CIS (7 mg/kg) on day 14. Oxidative stress markers, inflammatory markers and endoplasmic reticulum stress markers of ovarian tissues, and ovarian SIRTuin-1 (SIRT-1) were analyzed. Histopathological examination of ovaries and capase-9 immunohistochemical staining were also evaluated. CIS significantly increased ovarian oxidative stress markers, ER stress markers and reduced both AMH levels and SIRT-1 expression. Histopathological findings showed ovarian toxicity, necrosis and positive capase-9 immuno-expression. EMPA significantly decreased both oxidative stress and ER stress biomarkers with a significant improvement in the histopathological findings and a decrease in caspase-9 immuno-expression.Accordingly, EMPA protected against CIS-induced ovarian damage by activating both the SIRT-1/NRF2 /caspase-9 pathway and reducing ER stress.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enterogenic dementia: defining the gut-brain axis and the role of inflammatory bowel disease in cognitive impairment.","authors":"Faisal Alshammari, Hayder M Al-Kuraishy, Mustafa M Shokr, Marios Papadakis, Athanasios Alexiou, Gaber El-Saber Batiha","doi":"10.1007/s10787-025-01940-6","DOIUrl":"https://doi.org/10.1007/s10787-025-01940-6","url":null,"abstract":"<p><p>Dementia is a clinical syndrome due to brain neurodegeneration and associated oxidative stress and neuroinflammation. Chronic inflammatory and immunological diseases are associated with the development of dementia due to the development of neuroinflammation and synaptic dysfunction. Dementia is commonly related to inflammatory bowel disease (IBD), which may be named as an enterogenic dementia, which results from gut dysbiosis, systemic inflammation, and neuroinflammation. IBD is regarded as a potential risk factor for the development and progression of dementia, known as enterogenic dementia, through different mechanisms such as alteration of the gut-brain axis and gut dysbiosis. However, the precise mechanism linking IBD and dementia is not fully elucidated and remains elusive. In this perspective, we try to discuss the mechanisms for the development and progression of enterogenic dementia in relation to IBD and gut dysbiosis.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}