
The primary factor in Alzheimer's disease (AD) is the excessive presence of β-amyloid protein (Aβ) in the brain, with a significant amount derived from platelets in peripheral blood. The connection between peripheral Aβ levels and brain aggregation, particularly its role in AD pathology and its relation to tau tangles, is unclear. The recent approval of anti-Aβ monoclonal antibodies for AD treatment suggests that peripheral blood Aβ influences brain Aβ burden and contributes to AD development. The role of peripheral innate immune cells in AD is still uncertain. This review summarizes recent findings on peripheral blood Aβ and innate immune cells in AD pathogenesis, proposing that peripheral blood Aβ impacts AD development through its influence on innate immune cells.
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