Is Amyloid-β in Peripheral Blood Implicated in Alzheimer’s Disease through Inflammatory Mechanisms?
The presence of Amyloid-β in the bloodstream, blood vessels, and brain has been linked to Alzheimer’s disease. Recent studies have suggested that excessive peripheral blood Amyloid-β may contribute to the chronic inflammation associated with Alzheimer’s disease. This inflammation, known to play a role in the progression of the disease, is thought to be triggered by Aβ levels in the peripheral blood. Furthermore, research has shown that reducing the levels of peripheral blood Amyloid-β can lead to a decrease in brain Amyloid-β burden, suggesting a potential role for peripheral blood Aβ in the pathology of Alzheimer’s disease. To better understand the link between peripheral blood Aβ and Alzheimer’s disease, recent studies have focused on the role of peripheral innate immune cells in the pathogenesis of the disease. Findings indicate that in the early stages of Alzheimer’s disease, peripheral Aβ can activate these immune cells, leading to the secretion of inflammatory cytokines and molecules that affect the blood-brain barrier. Additionally, in the late stages of the disease, peripheral Aβ may impact the inflammatory processes and lead to an increase in proinflammatory cytokines, promoting the recruitment of more peripheral innate immune cells to the brain. This suggests that peripheral blood Aβ may contribute to Alzheimer’s disease through inflammatory mechanisms. This review summarizes recent research on the roles of peripheral blood Aβ and peripheral innate immune cells in the pathogenesis of Alzheimer’s disease, shedding light on potential new avenues for therapeutic intervention.
