A protein that suppresses division in brain cells has been found to apply “the brakes” on the dementia that accompanies Alzheimer's disease.
But when it fails, there's no holding back dementia, says a new study that contends that the discovery could open the way to new ways of treating Alzheimer's disease, which affects half the population over 85.
Determining the protein's previously unsuspected role in Alzheimer's is an important piece of the puzzle and it brings a new perspective to what causes the disease.
“It changes the logic from a search for a trigger that kicks off the dementia to the failure of a safety that has suppressed it,” said Karl Herrup of the State University of New Jersey, who led the study.
Looking at Alzheimer's through the lens of cancer, Herrup sees the rampant cell division associated with cancer mirrored in Alzheimer's-related dementia.
In cancer, uncontrollable cell division enables the disease to overwhelm normal body cells. Adult neurons, or nerve cells, do not normally divide.
Herrup's team experimented with a protein family known as cyclin-dependent kinases (Cdk). These enzymes power the cell cycle, driving it forward through its various phases.
The scientists focused on one particular kinase -- Cdk5 -- termed “an atypical kinase” because they could find no involvement in propelling the cell cycle.
They found that while it appears to be inert as a cell cycle promoter, Cdk5 in the nervous system actually functions to hold the cell cycle in check.
“Its mere presence helps protect the brain,” Herrup said. “What we discovered is that Cdk5 acts as a brake, not a driver.”
The findings of the study have been reported in the latest edition of the Proceedings of the National Academy of Sciences.