A loss of protein function in neurons may lead to Alzheimer’s Disease.

Rutgers researcher Karl Herrup and colleagues at Case Western Reserve University have discovered that a protein that suppresses cell division in brain cells effectively “puts the brakes” on the dementia that comes with Alzheimer’s disease (AD). When the brakes fail, dementia results.

It is estimated that Alzheimer’s disease may affect up to half the U.S. population over the age of 85.

Determining the protein’s previously unsuspected role in AD is an important piece of the puzzle and it brings a new perspective to the basis of AD. “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,” Herrup said.

The researchers reported their findings in the in the June 24 Proceedings of the National Academy of Sciences (PNAS).

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 ejection of Cdk5 out of the nucleus is probably related to the changed chemistry of the Alzheimer’s brain and chronic inflammation that accompanies AD,” Herrup said.

Source
Eureka Alert