Does Peripheral Blood Amyloid- β Contribute to Alzheimer ' s Disease via Inflammatory Mechanisms?

Amyloid-β is found in the bloodstream and blood vessels as well as in the brain, and an increase in this peripheral amyloid-β is noted in Alzheimer's disease patients who exhibit the characteristic amyloid-β aggregates in their brains. Current thinking is that there is a dynamic equilibrium between amyloid-β in the brain and body, and based on this view some success has been achieved in reducing amyloid-β in the brain by clearing amyloid-β in the rest of the body. Does this peripheral amyloid-β contribute to the onset of Alzheimer's disease in other ways, however? Researchers here suggest that it may increase the burden of systemic chronic inflammation, known to be involved in Alzheimer's disease pathology. A key pathological factor of Alzheimer's disease (AD), the most prevalent form of age-related dementia in the world, is excessive β-amyloid protein (Aβ) in extracellular aggregation in the brain. And in the peripheral blood, a large amount of Aβ is derived from platelets. So far, the causality between the levels of peripheral blood Aβ and its aggregation in the brain, particularly the role of the peripheral blood Aβ in the pathology of AD, is still unclear. And the relation between the peripheral blood Aβ and tau tangles of brain, another crucial pathologic factor contributing to the pathogenesis of AD, is also ambiguous. More recently, the anti-Aβ monoclonal antibodies are approved for treatment of AD patients through declining the peripheral...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs