Abstract
During Alzheimer's disease (AD) pathogenesis, Abeta peptides accumulate, build plaques in the brain and lead to neurodegeneration and thus, cognitive impairment. Plaque formation depends not solely on the amount of Abeta which is produced, but also on the effective removal of the peptide. The latter process is predominantly accomplished by microglia, the resident immune cells of the central nervous system (CNS). However, it has been shown that upon chronic exposure to Abeta microglia become inactivated, leading to insufficient clearance.
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