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著者: Young-Jung Lee, Sang Bae Han, Sang-Yoon Nam, Ki-Wan Oh, Jin Tae Hong
雑誌名: Arch Pharm Res. 2010 Oct;33(10):1539-56. doi: 10.1007/s12272-010-1006-7. Epub 2010 Oct 30.
Abstract/Text
Alzheimer's disease (AD) is the most common form of dementia. It is characterized by extracellular deposition of a specific protein, beta-amyloid peptide fibrils, and is accompanied by extensive loss of neurons in the brains of affected individuals. Although the pathophysiologic mechanism is not fully established, inflammation appears to be involved. Neuroinflammation has been known to play a critical role in the pathogenesis of chronic neurodegenerative disease in general, and in AD in particular. Numerous studies show the presence of a number of markers of inflammation in the AD brain: elevated inflammatory cytokines and chemokines, and accumulation of activated microglia in the damaged regions. Epidemiological studies have shown that long-term use of non-steroidal anti-inflammatory drugs suppresses the progression of AD and delays its onset, suggesting that there is a close correlation between neuroinflammation and AD pathogenesis. The aim of this review is (1) to assess the association between neuroinflammation and AD through discussion of a variety of experimental and clinical studies on AD and (2) to review treatment strategies designed to treat or prevent AD.
PMID 21052932 Arch Pharm Res. 2010 Oct;33(10):1539-56. doi: 10.1007/s12272-010-1006-7. Epub 2010 Oct 30.
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