作者: Stefan Prokop , Kelly R. Miller , Frank L. Heppner
DOI: 10.1007/S00401-013-1182-X
关键词:
摘要: The identification of microglia-associated, neurological disease-causing mutations in patients, combined with studies mouse models has highlighted microglia, the brain’s intrinsic myeloid cells, as key modulators pathogenesis and disease progression neurodegenerative diseases. In Alzheimer’s (AD) particular, activation accumulation microglial cells around β-Amyloid (Aβ) plaques long been described is believed to result chronic neuroinflammation—a term that, despite being commonly used, lacks a precise definition. This seemingly directed response microglia amyloid deposits conflicts fact that increasing buildup Aβ not inhibited by these during progression. While recent evidence suggests lose their beneficial function course AD may even acquire “toxic” phenotype over time, also simply be an appropriate trigger induce phagocytosis degradation vivo. As experimental indicated importance pathogenesis, future efforts aimed at tackling this via utilization or modulation factors therefrom appear exciting challenging research front.