A recent report from researchers at the Massachusetts General Hospital which identifies a protein that aids the immune system in the removal of A-beta protein from the brain, could lead to new treatments of Alzheimer’s disease. According to cocorresponding author of the report, Dr. Joseph Eli Khoury of the Center for Immunology and Inflammatory Diseases in the MGH Division of Infectious Diseases, their team identified a receptor protein which mediates the clearance of soluble A-beta protein from the brain by cells of the natural, pre-existing immune system. Soluble amyloid-beta proteins occur naturally in the brain, but come together and form plaques as a benchmark of Alzheimer’s disease. The scientists found that a mouse model with Alzheimer’s disease that indicated having a deficiency of the receptor experienced greater A-beta deposition and an accelerated death. This is held in contrast to the findings that an up-regulating expression of the receptor led to the enhancement of A-beta clearance from the brain.
The brain’s immune system seems to play a double role in neurodegenerative disorders such as Alzheimer’s disease. In the early stages of the disease, cells like microglia, monocytes, and macrophages offer resistance by engulfing and removing foreign materials from the brain, including buildups of amyloid beta. But as the disease progresses, the A-beta plaques grow larger and the cells lose their ability to absorb the excess of A-beta. This causes cells to release inflammatory chemicals which can cause further harm to the brain. Identifying the involvement of the receptor Scara1 in the uptake of A-beta by monocytes and macrophages, the team confirmed that Scara1 was the major receptor for recognition and clearance of A-beta by the immune system. Research found that a mouse with Alzheimer’ that lacked one or both copies of the Scara1 gene died earlier than a mouse with two functioning copies of the gene. The team treated cultured immune cells with Protollin, a compound used to enhance immune response within vaccines. When the cells were exposed to Protollin, they tripled the expression of Scara1, while also increasing a protein that attracts immune cells. When they added microglia stimulated with Protollin to brain samples from the Alzheimer’s mice, it reduced the size and amount of A-beta deposits in the hippocampus region of the brain.
1) “Increased expression of Scara1 protein might impede progression of Alzheimer’s disease: Study” (2013, July 2http://www.news-medical.net/news/20130702/Increased-expression-of-Scaraprotein-might-impede-progression-of-Alzheimers-disease-Study.aspxnd) News-Medical.net. Retrieved July 7th, 2013 from http://www.news-medical.net/news/20130702/Increased-expression-of-Scara1-protein-might-impede-progression-of-Alzheimers-disease-Study.aspx
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