National Institute on Aging, NIH
In June, the Food and Drug Administration approved the first drug designed to slow the progression of Alzheimer’s disease. The drug, called aducanumab, clears amyloid plaques — clumps of brain proteins that are characteristic of Alzheimer’s disease. Proponents of the drug say that amyloid plaques are toxic, and that they lead to brain inflammation and the loss of brain cells, causing cognitive impairment.
But critics say there is scant evidence that the drug actually helps people with Alzheimer's, and not all scientists agree that amyloid plaques cause the disease, though there is a correlation. In fact, some people with amyloid plaques do not show cognitive decline.
In new study, University of Cincinnati researchers sought to understand this apparent paradox. Their idea is maybe the cause of Alzheimer’s is not an accumulation of these protein clumps, but rather a decrease in their precursor: soluble un-clumped amyloid proteins in the brain. Soluble amyloid proteins have a number of important jobs in brain function, including brain development and protecting brain cells from premature death.
To test this idea, the researchers looked at soluble amyloid protein levels in people with varying stages of cognitive decline. They found that healthy individuals with amyloid plaques in their brains still had high levels of the soluble amyloid protein. Dementia was much more related to low soluble protein levels than it was to high levels of amyloid plaques. These results add to the evidence that plaques may not be the direct cause of Alzheimer’s, and they calls into question the FDA’s decision to approve aducanumab.