One of Aubrey de Grey's Strategies for Engineered Negligible Senescence (SENS) aims to improve the ability of cells to remove accumulated intracellular trash. Accumulation of damaged proteins and other cellular components is one of the causes of aging. With this thought it mind it is interesting to look at research research where by turning up the parkin protein (whose malfunction is implicated in Parkinson's Disease) UCLA scientists were able to extend the lives of fruit flies.
UCLA life scientists have identified a gene previously implicated in Parkinson's disease that can delay the onset of aging and extend the healthy life span of fruit flies. The research, they say, could have important implications for aging and disease in humans.
The gene, called parkin, serves at least two vital functions: It marks damaged proteins so that cells can discard them before they become toxic, and it is believed to play a key role in the removal of damaged mitochondria from cells.
"Aging is a major risk factor for the development and progression of many neurodegenerative diseases," said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research. "We think that our findings shed light on the molecular mechanisms that connect these processes."
In the research, published today in the early online edition of the journal Proceedings of the National Academy of Sciences, Walker and his colleagues show that parkin can modulate the aging process in fruit flies, which typically live less than two months. The researchers increased parkin levels in the cells of the flies and found that this extended their life span by more than 25 percent, compared with a control group that did not receive additional parkin.
"In the control group, the flies are all dead by Day 50," Walker said. "In the group with parkin overexpressed, almost half of the population is still alive after 50 days. We have manipulated only one of their roughly 15,000 genes, and yet the consequences for the organism are profound."
Engineering mice and other organisms to turn up their parkin seems like an obvious next step. But achieving such a large benefit might be harder for humans. Some of our accumulated intracellular trash not not be removable by the proteins we have in our cells. We accumulate so many kinds of trash over many years that the ones left in our cells might have characteristics that make them hard to remove. Hence Aubrey's interest in finding enzymes from other organisms that can cut up and remove intracellular trash.
We most need intracellular trash removal in our brains because we need to preserve our neurons. By contrast, we will eventually be able to grow replacements for most other organs.
|Share |||Randall Parker, 2013 May 09 10:35 PM|