Autoantibodies May Play Role in Alzheimer’s
- By BSTQ Staff
New research demonstrates how 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 research also identifies a key mechanism in the development of Alzheimer’s that mirrors a process that is common in such autoimmune disorders as rheumatoid arthritis.
Conducted at the University of Medicine and Dentistry of New Jersey- School of Osteopathic Medicine (UMDNJ-SOM), the research 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. In addition, they demonstrated that a specific type of protein, PTCD2, which has been shown to be a potent biomarker for Alzheimer’s, was present in citrullinated form in the neuron cells of the Alzheimer’s disease brain samples.
These results suggest that when the brain 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. This same protein citrullination process has been linked to the development of autoantibodies in rheumatoid arthritis, one of the most common forms of autoimmune disease. The study appears online in the Journal of Autoimmunity.
