Blocking Alzheimer’s Disease Process by Blocking Specific Protein

The strategy is based on unclogging and removing the toxic debris that gathers in patients’ brains, by suppressing activity of a little-known regulator protein called CD33.

“Too much CD33 appears to promote late-onset Alzheimer’s by preventing support cells from clearing out toxic plaques, key risk factors for the disease,” explained Rudolph Tanzi, PhD, of Massachusetts General Hospital (Boston, MA, USA) and Harvard University (Cambridge, MA, USA), a grantee of the US National Institutes of Health’s (NIH; Bethesda, MD, USA) National Institute of Mental Health (NIMH) and National Institute on Aging (NIA).“Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.”

Dr. Tanzi and colleagues reported their findings April 25, 2013, in the journal Neuron. Variation in the CD33 gene appeared as one of four prime suspects in the largest genome-wide dragnet of Alzheimer's-affected families, reported by Dr. Tanzi and colleagues in 2008.

The scientists found over-expression of CD33 in support cells, called microglia, in postmortem brains from patients who had late-onset AD, the most typical form of the disorder. The more CD33 protein on the cell surface of microglia, the more beta-amyloid proteins and plaques had accumulated in their brains. Moreover, the researchers discovered that brains of people who inherited a version of the CD33 gene that protected them from AD noticeably exhibited reduced amounts of CD33 on the surface of microglia and less beta-amyloid.