Exercise suppresses neuroinflammation for alleviating Alzheimer's disease

• Published in: Journal of neuroinflammation 2023-03, Vol.20 (1), p.76-76, Article 76
• Main Authors: Wang, Minghui, Zhang, Hu, Liang, Jiling, Huang, Jielun, Chen, Ning
• Format: Article
• Language: English
• Subjects: Alzheimer Disease; Alzheimer's disease; Analysis; Animal research; Animals; Biomarkers; Brain; Care and treatment; Central nervous system; Clinical trials; Cognitive ability; Dementia; Diagnosis; Disease prevention; Endoplasmic reticulum; Epidemiology; Exercise; Exercise therapy; Glycoproteins; Hippocampus; Humans; Hypotheses; Immune response; Inflammasomes; Inflammasomes - metabolism; Inflammation; Inflammation - metabolism; Microglia; Microglia - metabolism; Neurodegeneration; Neurodegenerative diseases; Neurodegenerative Diseases - metabolism; Neurofibrillary tangle; Neurofibrillary Tangles - metabolism; Neurogenesis; Neuroinflammation; Neuroinflammatory Diseases; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism; Oxidative stress; Pathogenesis; Patient outcomes; Peptides; Proteins; Pyrin protein; Review; Senile plaque; Senile plaques
• ISSN: 1742-2094; 1742-2094
• DOI: 10.1186/s12974-023-02753-6

Alzheimer's disease (AD) is a chronic neurodegenerative disease, with the characteristics of neurofibrillary tangle (NFT) and senile plaque (SP) formation. Although great progresses have been made in clinical trials based on relevant hypotheses, these studies are also accompanied by the emergence of toxic and side effects, and it is an urgent task to explore the underlying mechanisms for the benefits to prevent and treat AD. Herein, based on animal experiments and a few clinical trials, neuroinflammation in AD is characterized by long-term activation of pro-inflammatory microglia and the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes. Damaged signals from the periphery and within the brain continuously activate microglia, thus resulting in a constant source of inflammatory responses. The long-term chronic inflammatory response also exacerbates endoplasmic reticulum oxidative stress in microglia, which triggers microglia-dependent immune responses, ultimately leading to the occurrence and deterioration of AD. In this review, we systematically summarized and sorted out that exercise ameliorates AD by directly and indirectly regulating immune response of the central nervous system and promoting hippocampal neurogenesis to provide a new direction for exploring the neuroinflammation activity in AD.