New Clues on CD33 Protein’s Role in Alzheimer’s May Be Key to Treatment, Researchers Say

New Clues on CD33 Protein’s Role in Alzheimer’s May Be Key to Treatment, Researchers Say
Researchers have discovered a likely reason why the most common form of the CD33 protein is a risk factor for Alzheimer's disease, a finding that could open new therapeutic avenues targeting the protein, a study reports. The protein stops brain immune cells known as microglia from wiping out beta-amyloid clumps, which are seen as a root cause of Alzheimer's. Findings from the study, "Repression of phagocytosis by human CD33 is not conserved with mouse CD33," could result in treatment strategies that target CD33 and  shift microglia function to a protective state rather than a harmful one. The study was published in the journal Communications Biology. CD33 is a surface receptor protein found in immune cells circulating in the blood as well as in specialized brain-resident immune cells called microglia. This receptor has been implicated in the risk of Alzheimer's. Prior studies have shown that a rare form of CD33 — present in fewer than 10% of the population — makes people less likely to develop Alzheimer's disease. In contrast, the CD33 version most frequently found in people seems to have the opposite effect, contributing to Alzheimer's susceptibility. Increased levels of CD33 have been found in the brains of people with Alzheimer's and correlated with disease severity and the overall load of amyloid plaques in the brain — one of the underlying causes of the disease. "Immune cells in the brain, called microglia, play a critical role in Alzheimer's disease," study author Matthew Macauley, PhD, professor at the University of Alberta, said in a press release. A growing body of evidence suggests that CD33 controls how microglial cells — the immune cells of the brain — work, impairing their ability to clear toxic beta-amyloid protein fragments and leading
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