In Alzheimer’s Disease, Adaptive Immune System Plays Important Role

In Alzheimer’s Disease, Adaptive Immune System Plays Important Role
Researchers have discovered that a genetic elimination of peripheral immune cell populations leads to a more rapid development of amyloid brain plaques (which are present in Alzheimer's patients), worsening of neuroinflammation, and dysfunction of microglial activity. The study, “The adaptive immune system restrains Alzheimer’s disease pathogenesis by modulating microglial function,” was published in Proceedings of the National Academy of Sciences. Alzheimer’s disease (AD), the leading cause of age-related neurodegeneration, is characterized by two protein aggregate structures, amyloid-β (Aβ) plaques and neurofibrillary tangles. Usually, microglia -- immune system cells that act in the central nervous system -- respond and destroy these plaques, but eventually develop a more pro-inflammatory role and contribute to the chronic neuroinflammation observed in Alzheimer's disease. Research has long focused on and uncovered the role of innate immunity in Alzheimer's development, but the adaptive immune system’s role remains largely unknown. The number of clinical trials studying vaccination strategies for Alzheimer's indicates that the adaptive immunity may indeed be a significant player in Alzheimer’s. To investigate if the adaptive immune system, specifically immune B- and T-cells, plays a role in Alzheimer's pathogenesis, researchers developed a genetically modified mouse model of AD that lacked T, B, and natural killer (NK) cells. The researchers observed that these mice had a twofold increase in amyloid plaque accumulation when compared to normal mice. Gene expression analyses indicated altered innat
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