The only known genetic risk factor for Alzheimer's disease slows down the brain's ability to export a toxic protein known as amyloid-beta that is central to the damage the disease causes, scientists have found.
The research, published Nov. 13 by the Journal of Clinical Investigation, provides new clues into the workings of a protein known as apolipoprotein E4, or ApoE4. People who carry two copies of the gene have roughly eight to 10 times the risk of getting Alzheimer's disease than people who do not.
The new results mark a step toward resolving a longstanding question that scientists have had about exactly how ApoE4 increases a person's risk for the disease. The findings point to differences in the way that amyloid-beta is removed from the brain depending on which ApoE protein is involved.
Scientists found that when ApoE4 is present, the brain is less efficient at ridding itself of the toxic material, because a molecule that is much slower at removing the substance becomes much more involved.
Biogerontologist Aubrey de Grey argues that one of the major causes of cellular aging is the accumulation of toxic junk inside of aging cells. The body lacks enzymes to break down some kinds of intracellular junk. Therefore Aubrey argues for development of therapies to transplant into aging human cells the genes for enzymes that break down intracellular junk in other species. This report that Alzheimer's risk is boosted by a gene involved in intracellular trash removal underscores the importance of intracellular trash accumulation in brain aging. If we could remove more of the trash that accumulates in cells as we age then we wouldn't age as rapidly.
|Share |||Randall Parker, 2008 November 14 12:58 AM Brain Alzheimers Disease|