Amyloid- β Biochemistry as a Cause of Blood-Brain Barrier Leakage in Alzheimer ' s Disease

Alzheimer's disease is a complex degenerative failure of a complex system, the brain. This complexity is illustrated by the continuing debate over which of the many identified mechanisms are the primary cause. Is it amyloid-β aggregation, or some aspect of the halo of biochemistry associated with that aggregation, or is it chronic inflammation, or cellular senescence in supporting cells of the brain, or vascular dysfunction and leakage of the blood-brain barrier, or neurofibrillary tangles, or the presence of persistent viruses. All of these mechanisms interact with one another, and the direction of causation between any specific pair of mechanisms is also up for debate. Researchers are in many cases challenged by the inability to affect one mechanism in isolation of the others; even immunotherapies to clear amyloid-β have side-effects on tissues and the immune system. In today's open access paper, researchers point out that most Alzheimer's patients exhibit cerebral amyloid angiopathy, deposition of amyloid-β into blood vessel walls leading to dysfunction, leakage, and rupture of microvessels. This results in damage to surrounding brain tissue and passage of inappropriate cells and molecules into the brain, provoking inflammation, among other consequences. The paper delves into mechanisms by which amyloid-β aggregation might cause dysfunction of the blood-brain barrier wrapping blood vessels in the brain and thus also the problems that arise from leakage of the bl...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs