期刊
JOURNAL OF NEURAL TRANSMISSION
卷 117, 期 8, 页码 961-970出版社
SPRINGER WIEN
DOI: 10.1007/s00702-010-0422-7
关键词
Brain; Innate immunity; Neurodegeneration; Mononuclear phagocyte; Microglia; Astrocyte
资金
- NIA/NIH Pathway to Independence'' [5R00AG029726-03, 5R00AG029726-04]
- Gary and Cheryl Justice
Alzheimer's disease (AD) is a progressive and incurable neurodegenerative disorder clinically characterized by cognitive decline involving loss of memory, reasoning and linguistic ability. The amyloid cascade hypothesis holds that mismetabolism and aggregation of neurotoxic amyloid-beta (A beta) peptides, which are deposited as amyloid plaques, are the central etiological events in AD. Recent evidence from AD mouse models suggests that blood-borne mononuclear phagocytes are capable of infiltrating the brain and restricting beta-amyloid plaques, thereby limiting disease progression. These observations raise at least three key questions: (1) what is the cell of origin for macrophages in the AD brain, (2) do blood-borne macrophages impact the pathophysiology of AD and (3) could these enigmatic cells be therapeutically targeted to curb cerebral amyloidosis and thereby slow disease progression? This review begins with a historical perspective of peripheral mononuclear phagocytes in AD, and moves on to critically consider the controversy surrounding their identity as distinct from brain-resident microglia and their potential impact on AD pathology.
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