Ameliorative action of probiotics on the neurotoxicological effect of Aluminium chloride and D-galactose DOI Creative Commons
Vaishali Dasriya, Manorama Kumari, Soniya Ranveer

et al.

Deleted Journal, Journal Year: 2025, Volume and Issue: 2(1)

Published: April 14, 2025

Language: Английский

Implicative role of cytokines in neuroinflammation mediated AD and associated signaling pathways: Current progress in molecular signaling and therapeutics DOI
Sneha Kumari,

Rishika Dhapola,

Prajjwal Sharma

et al.

Ageing Research Reviews, Journal Year: 2023, Volume and Issue: 92, P. 102098 - 102098

Published: Oct. 30, 2023

Language: Английский

Citations

16

Natural products as potential modulators of pro-inflammatory cytokines signalling in Alzheimer's disease DOI Creative Commons
Vikas Yadav,

C Mythri,

Murali Kumarasamy

et al.

Brain Behavior and Immunity Integrative, Journal Year: 2024, Volume and Issue: 5, P. 100048 - 100048

Published: Jan. 1, 2024

Alzheimer's disease (AD) is the most common neurodegenerative disorder and primary cause of dementia in elderly population. Previous studies have suggested that numerous processes are involved development AD, such as accumulation amyloid-β (Aβ) peptides, hyperphosphorylated tau (τ) proteins, pro-inflammatory cytokine signalling pathway, which results neuroinflammation. Elevated microglial activation expression cytokines, reactive oxygen species (ROS), nuclear factor kappa B (NF-κB) also participate process AD. Together, these contribute significantly to progression. To slow progression, this review focuses on molecular mechanisms influenced by natural compounds. Natural products many known beneficial health effects diseases, specifically because their anti-inflammatory properties. capable decreasing symptoms alleviating several including thus attracting attention scientific community pharmaceutical industry. This therapeutic potential abundant bioactive compounds, can modulate

Language: Английский

Citations

5

Alzheimer’s disease and its associated risk of bone fractures: a narrative review DOI Creative Commons

Bingna Zhou,

Qian Zhang, Mei Li

et al.

Frontiers in Endocrinology, Journal Year: 2023, Volume and Issue: 14

Published: Aug. 9, 2023

Background Alzheimer’s disease (AD) is a neurodegenerative disorder that the major cause of dementia in aged population. Recent researches indicate patients with AD have significantly increased fracture risk, but pathological mechanisms are still unclear. Objective We systematically reviewed studies regarding bone risk to uncover links between pathologies osteoporosis and AD. Methods searched literature using databases PubMed, Web Science, Embase Cochrane Library. Studies were included if they evaluated explored pathogenesis prevention fractures these patients. Results had higher than age-matched controls. Multiple factors contributed patients, including direct effects amyloid pathology on cells, abnormal brain-bone interconnection, Wnt/β-catenin signalling deficits, reduced activity, high falls frailty, chronic immune activity. Exercise, fortified nutrition beneficial for reducing However, efficacy anti-osteoporotic agents preventing should be further as corresponding clinical very scarce. Conclusion decreased mineral density owing multiple factors. Assessment agents’ urgently needed.

Language: Английский

Citations

13

Advances in Blood Biomarkers for Alzheimer’s Disease: Ultra-Sensitive Detection Technologies and Impact on Clinical Diagnosis DOI Open Access
Yi Zhang,

Kefan Bi,

Linfu Zhou

et al.

Degenerative Neurological and Neuromuscular Disease, Journal Year: 2024, Volume and Issue: Volume 14, P. 85 - 102

Published: July 1, 2024

Abstract: Alzheimer's disease has escalated into a critical public health concern, marked by its neurodegenerative nature that progressively diminishes cognitive abilities. Recognized as continuously advancing and presently incurable condition, AD underscores the necessity for early-stage diagnosis interventions aimed at delaying decline in mental function. Despite proven efficacy of cerebrospinal fluid positron emission tomography diagnosing AD, their broader utility is constrained significant costs invasive these procedures. Consequently, innovation blood biomarkers such Amyloid-beta, phosphorylated-tau, total-tau et al, distinguished high sensitivity, minimal invasiveness, accessibility, cost-efficiency, emerges promising avenue diagnosis. The advent ultra-sensitive detection methodologies, including single-molecule enzyme-linked immunosorbent assay immunoprecipitation-mass spectrometry, revolutionized plasma biomarkers, supplanting previous low-sensitivity techniques. This rapid advancement technology facilitates more accurate quantification pathological brain proteins AD-associated bloodstream. manuscript meticulously reviews landscape current research on immunological markers anchored National Institute Aging—Alzheimer's Association AT(N) framework. It highlights selection forefront technologies now integral to assessing markers. Additionally, this review examines crucial pre-analytical processing steps samples significantly impact outcomes addresses practical challenges faced during clinical testing. These discussions are enhancing our comprehension refining diagnostic precision using blood-based biomarkers. aims shed light potential avenues improvement techniques employed detecting investigating thereby contributing field research. Keywords: disease, blood, technologies,

Language: Английский

Citations

4

Glyphosate exposure exacerbates neuroinflammation and Alzheimer’s disease-like pathology despite a 6-month recovery period in mice DOI Creative Commons
Samantha K. Bartholomew, Wendy Winslow, Ritin Sharma

et al.

Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)

Published: Dec. 4, 2024

Language: Английский

Citations

4

Mechanisms and Emerging Regulators of Neuroinflammation: Exploring New Therapeutic Strategies for Neurological Disorders DOI Creative Commons

Mi Eun Kim,

Jun Sik Lee

Current Issues in Molecular Biology, Journal Year: 2024, Volume and Issue: 47(1), P. 8 - 8

Published: Dec. 26, 2024

Neuroinflammation is a complex and dynamic response of the central nervous system (CNS) to injury, infection, disease. While acute neuroinflammation plays protective role by facilitating pathogen clearance tissue repair, chronic dysregulated inflammation contributes significantly progression neurodegenerative disorders such as Alzheimer's disease, Parkinson's Multiple Sclerosis. This review explores cellular molecular mechanisms underlying neuroinflammation, focusing on roles microglia, astrocytes, peripheral immune cells. Key signaling pathways, including NF-κB, JAK-STAT, NLRP3 inflammasome, are discussed alongside emerging regulators non-coding RNAs, epigenetic modifications, gut-brain axis. The therapeutic landscape evolving, with traditional anti-inflammatory drugs like NSAIDs corticosteroids offering limited efficacy in conditions. Immunomodulators, gene RNA-based therapeutics, stem cell methods have all shown promise for more specific effective interventions. Additionally, modulation metabolic states gut microbiota has emerged novel strategy regulate neuroinflammation. Despite significant progress, challenges remain translating these findings into clinically viable therapies. Future studies should concentrate integrated, interdisciplinary reduce slowing disorders, providing opportunities revolutionary advances CNS

Language: Английский

Citations

4

Linking evidence for targeted blood biomarkers in post-stroke cognitive impairment and dementia DOI Creative Commons
Jie Hong,

Katherine T Mun,

Kyle C. Kern

et al.

Frontiers in Stroke, Journal Year: 2025, Volume and Issue: 3

Published: Jan. 7, 2025

With improvements in acute stroke treatment and more patients surving the period, identification prognostication of post-stroke disability is paramount. Post-stroke cognitive impairment dementia (PSCID) severely impacts morbidity mortality survivors. While clinical factors imaging are useful identifying at risk for PSCID, blood-based biomarkers sorely needed to provide cost-effective greatest risk. Furthermore, can inform biologic basis PSCID lead potential targets. This narrative review attempts summarize currently available research on use fluid measure quantify using a framework proposed DISCOVERY Network study PSCID. In this framework, blood divided into broad pathologic categories including inflammation, neurodegeneration, neuroaxonal injury, vascular injury. Key that have been as relevant include interleukin-6, C-reactive protein, β-amyloid 42:40 ratio, neurofilament light chain, 10 angiogenic molecules. Critical assessment prior studies includes defining sample collection period assess temporal pattern biomarker levels relation an incident event. addition comprehensive review, we performed protein-protein network analysis putative (surprisingly) find they exist highly connected interaction centered inflammatory neurodegenerative suggesting shared biology underlies pathogenesis Both literature point role combinatorial methodology enhance specificity sensitivity prognostic highlights emerging evaluating while also informing underlying creates synergy between dementia.

Language: Английский

Citations

0

Rebalancing Immune Interactions within the Brain-Spleen Axis Mitigates Neuroinflammation in an Aging Mouse Model of Alzheimer’s Disease DOI Creative Commons
Anna Cantone, Chiara Burgaletto, Giulia Di Benedetto

et al.

Journal of Neuroimmune Pharmacology, Journal Year: 2025, Volume and Issue: 20(1)

Published: Feb. 7, 2025

Alzheimer's disease (AD) is the most common cause of dementia worldwide, characterized by accumulation amyloid-β protein and hyperphosphorylated tau in brain. Neuroinflammation, resulting from chronic activation brain-resident innate immune cells as well enhanced peripheral leukocyte access across blood-brain barrier, crucially affects AD progression. In this context, TNFSF10, a cytokine substantially expressed brain, has been shown to modulate both adaptive branches response AD-related neuroinflammation. study, we explored whether TNFSF10-neutralizing treatment could represent tool re-balance overall overshooting inflammatory mouse model AD. Specifically, 3xTg-AD mice were treated sub-chronically with an anti-TNFSF10 monoclonal antibody for three months, then sacrificed at 15 months. TNFSF10 neutralization reduced expression marker CD86, inversely related levels anti-inflammatory CD206 brain mice, suggesting switch microglia towards neuroprotective phenotype. Similar results observed splenic macrophage population. Moreover, flow cytometry revealed significant decrease CD4+CD25+FOXP3+ T regulatory number CD11b+LY6Chigh proinflammatory monocytes spleen antibody. Finally, resulted lower count CD4+ CD8+ expressing PD1. The data suggest that system-targeted effectively restrain central inflammation rebalancing response, mitigating progression pathology.

Language: Английский

Citations

0

The neuroinflammatory effects of acrolein on human microglial HMC3 cells in Alzheimer’s disease DOI

Jeffrey A. Black,

Manogna Jarajapu, Bennett Schackmuth

et al.

International Journal of Environmental Studies, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 19

Published: Feb. 18, 2025

Language: Английский

Citations

0

Molecular Mechanism of Action of Abamectin on Human Microglia Clone 3 Cell Line DOI
Okan Sancer, Fatma Nihan Çankara, Ünal Şahin

et al.

Applied In Vitro Toxicology, Journal Year: 2025, Volume and Issue: 11(1), P. 16 - 20

Published: Feb. 20, 2025

Introduction: Abamectin (ABA) is an insecticide that commonly used in agricultural spraying. Although it known to have neurotoxic effects on living organisms the ecosystem and humans, details of these effects, including duration amount exposure, are not fully understood. The aim this study evaluate effect ABA exposure human microglia clone 3 (HMC3) cells. These cells were chosen because they suitable for modeling immunological functions such as cytokine production, cell migration, inflammation response.

Language: Английский

Citations

0