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, Год журнала: 2024, Номер 47(1), С. 8 - 8

Опубликована: Дек. 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

Язык: Английский

Zooming in on brain inflammation in Alzheimer’s disease DOI Creative Commons
Wiesje M. van der Flier, Michael T. Heneka

Brain, Год журнала: 2025, Номер 148(1), С. 1 - 2

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

1

Network Diffusion-Constrained Variational Generative Models for Investigating the Molecular Dynamics of Brain Connectomes Under Neurodegeneration DOI Open Access
Jiajia Xie, Raghav Tandon, Cassie S. Mitchell

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(3), С. 1062 - 1062

Опубликована: Янв. 26, 2025

Alzheimer’s disease (AD) is a complex and progressive neurodegenerative condition with significant societal impact. Understanding the temporal dynamics of its pathology essential for advancing therapeutic interventions. Empirical anatomical evidence indicates that network decoupling occurs as result gray matter atrophy. However, scarcity longitudinal clinical data presents challenges computer-based simulations. To address this, first-principles-based, physics-constrained Bayesian framework proposed to model time-dependent connectome during neurodegeneration. This diffusion segments pathological progression into discrete time windows optimizes distributions biomarker regression, conceptualized learning problem. The employs variational autoencoder-like architecture computational enhancements stabilize improve training efficiency. Experimental evaluations demonstrate meta-models outperform traditional static models. models were evaluated using both synthetic real-world MRI PET datasets measure amyloid beta, tau, glucose metabolism. successfully distinguishes normative aging from AD pathology. Findings provide novel support “decoupling” hypothesis reveal eigenvalue-based destabilization in AD. Future optimization model, integrated data, expected applications personalized medicine other diseases.

Язык: Английский

Процитировано

0

Anti-Neuroinflammatory Eremophilane Sesquiterpenoids from Marine-Derived Fungus Phoma sp. DXH009 DOI Creative Commons
Guanyu Yang, Mengfan Qin,

Mingbin Chen

и другие.

Marine Drugs, Год журнала: 2025, Номер 23(3), С. 94 - 94

Опубликована: Фев. 20, 2025

Three new eremophilane sesquiterpenoids (1–3), together with six known analogues, were isolated from the marine-derived fungus Phoma sp. DXH009. Their structures elucidated through detailed NMR and MS spectroscopic analysis, absolute configurations of 1–4 determined by conformational analysis quantum chemical TDDFT-ECD calculation. anti-neuroinflammatory activities evaluated using lipopolysaccharide (LPS)-induced BV2 microglial cells. The results indicated that compound 5 (dihydrosporogen AO-1) exhibited significant inhibitory effects on production nitric oxide (NO) levels (EC50 = 3.11 μM) less cytotoxicity, leading to a reversal effect in inducing microphage polarization LPS-treated These correlated suppressions canonical NF-κB pathway as well expression key neuroinflammatory markers, including COX2, TNF-α, IL-6, IL-1β. Correspondingly, treating LPS-induced mice efficiently ameliorated neuroinflammation tissues cortex hippocampus. findings suggest sesquiterpenoid could be potential candidate for development drugs.

Язык: Английский

Процитировано

0

NLRP3 inflammasome in neuroinflammation and central nervous system diseases DOI Creative Commons
Wen Xu, Yi Huang, Rongbin Zhou

и другие.

Cellular and Molecular Immunology, Год журнала: 2025, Номер unknown

Опубликована: Март 13, 2025

Abstract Neuroinflammation plays an important role in the pathogenesis of various central nervous system (CNS) diseases. The NLRP3 inflammasome is intracellular multiprotein complex composed innate immune receptor NLRP3, adaptor protein ASC, and protease caspase-1. activation can induce pyroptosis release proinflammatory cytokines IL-1β IL-18, thus playing a inflammatory responses. Recent studies have revealed that activated brain to neuroinflammation, leading further neuronal damage functional impairment, contributes pathological process neurological diseases, such as multiple sclerosis, Parkinson’s disease, Alzheimer’s stroke. In this review, we summarize neuroinflammation course CNS diseases discuss potential approaches target for treatment

Язык: Английский

Процитировано

0

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, Год журнала: 2024, Номер 47(1), С. 8 - 8

Опубликована: Дек. 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

Язык: Английский

Процитировано

3