Abstract
Agonistic autoantibodies (agAAB) for alpha-1 adrenoceptor were found in approx. 50% of patients with Alzheimer's disease. These antibodies activate the receptor and trigger the signal cascades similarly to how natural agonists do. The agAAB bond to the receptor is persistent and prolonged. This results in a non-physiological elevation of intracellular calcium. An animal model has shown that agAAB causes macrovascular and microvascular impairment in the vessels of the brain. Reduction in blood flow and the density of intact vessels was significantly demonstrated. The agAAB was removed through immunoadsorption in a small cohort of patients with Alzheimer's disease. Subsequent follow-up observations over 12-18 months noted stabilization of cognition levels.
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