期刊
CURRENT ALZHEIMER RESEARCH
卷 14, 期 8, 页码 870-882出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1567205014666170317113606
关键词
Neuroinflammation; cytokines; chemokines; amyloid precursor protein; beta-amyloid; TAU
资金
- Fundacao para a Ciencia e Tecnologia of the Ministerio da Educacao e Ciencia [PIDC/DTP-PIC/5587/2014]
- Feder funds through compete
- iBiMED [UID/BIM/04501/2013]
Background: Alzheimer's disease (AD) is the most common neurodegenerative disorder, neuropathologically characterized by aggregates of beta-amyloid peptides, which deposit as senile plaques, and of TAU protein, which forms neurofibrillary tangles. It is now widely accepted that neuroinflammation is implicated in AD pathogenesis. Method: Indeed, inflammatory mediators, such as cytokines and chemokines (chemotactic cytokines) can impact on the Alzheimer's amyloid precursor protein by affecting its expression levels and amyloidogenic processing and/or beta- amyloid aggregation. Additionally, cytokines and chemokines can influence kinases' activities, leading to abnormal TAU phosphorylation. To date there is no cure for AD, but several therapeutic strategies have been directed to prevent neuroinflammation. Anti-inflammatory, but also anti-amyloidogenic compounds, such as flavonoids were shown to favourably modulate some pathological events associated with neurodegeneration. Conclusion: This review focuses on the role of cytokines and chemokines in AD-associated pathologies, and summarizes the potential anti- inflammatory therapeutic approaches aimed at preventing or slowing down disease progression.
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