Autoantibodies in Alzheimer’s Disease

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Via ScienceDaily, an example of a more recent form of theory to explain the development of Alzheimer's disease: "dying or damaged brain cells release debris into the bloodstream and give rise to specific autoantibodies that appear to be reliable biomarkers for early diagnosis of Alzheimer's and other neurodegenerative diseases. The researchers also identify a key mechanism in the development of Alzheimer's that mirrors a process that is common in such autoimmune disorders as rheumatoid arthritis. ... human blood contains perhaps thousands of autoantibodies for clearing cellular debris, and that some of these autoantibodies can potentially be used to accurately diagnose neurodegenerative diseases ... The researchers focused on the role of enzymes, called PADs, in citrullination, a process that converts one type of amino acid into another (amino acids are the building blocks of proteins). After examining postmortem human brain tissue from individuals with Alzheimer's disease and healthy controls, the researchers found that neurons located in the area of the brain first affected by Alzheimer's disease accumulate both citrullinated proteins and a PAD enzyme. ... Their results suggest that when neuron cells die, they release their contents into the fluid that surrounds the brain. The cellular remains then enter the bloodstream and their presence generates the production of specific autoantibodies that target this neuronal debris. ... Our previous studies provided evidence that some of these autoantibodies may be able to return to the brain through breaches in the blood-brain barrier. Once there, they selectively bind to the surfaces of neurons, disrupting the function of the brain cells and accelerating the accumulation of beta amyloid deposits. This chronic cycle of protein-debris-generating autoantibodies that can then seep through the blood-brain barrier helps explain the long-term, progressive degeneration that results from Alzheimer's disease."

Link: http://www.sciencedaily.com/releases/2012/05/120522161338.htm