How Increased Parkin Gene Levels Can Delay the Aging Process

 


U C L-A researchers found that increasing park in levels in fruit F L I-E cells increased their lifespan by more than 25% in comparison to a control group that received no additional park in. 


A gene that had been linked to Parkinson's disease has been found to be able to prolong fruit F L I-E healthy lifespans and delay the onset of aging. They assert that the research may have significant repercussions for human aging and disease.


Park in, a gene, performs at least two essential functions: It is thought to play a significant role in the process of removing damaged mitochondria from cells and marking damaged proteins so that cells can discard them before they become toxic. 


David Walker, senior author of the study and U C L-A associate professor of integrative biology and physiology, stated, "Aging is a major risk factor for the development and progression of many neurodegenerative diseases". We believe that our findings provide insight into the molecular mechanisms by which these processes are connected. 


His colleagues demonstrate in the study, which was published in the early online edition of the journal Proceedings of the National Academy of Sciences, that Parkinson's is able to alter the aging process in fruit F L I-E, which typically live for less than two months. When compared to a control group that received no additional park in, the researchers found that increasing park in levels in the F L I-E cells increased their lifespan by more than 25%


The onset and progression of Parkinson's disease and other age-related diseases may be slowed down by treatments that increase Parkinson's gene expression. A-N I-L R-A N-A, a postdoctoral researcher in Walker's lab, says, "They live significantly longer while remaining healthy, active, and fertile by simply increasing the levels of park in"


The Garbage Men In Our Cells Go On Strike

Proteins that have been misfolded or damaged build up in our cells as we age. Park in aids in the identification of damaged proteins for disposal. Mitochondria become less productive and less dynamic as we age. Alzheimer's, Parkinson's, and other neurodegenerative diseases are linked to decreased mitochondrial activity


If Park In Is Good, Is More Park In Even Better?

Researchers have discovered that fruit flies can live longer when their levels of the gene protein are elevated. Human aging can be studied using the fruit fly as a model because humans also have the Parkinson gene.


While the biologists increased park in activity in every fruit fly cell, R-A N-A only increased park in expression in the nervous system in an experiment. The flies also lived longer as a result of that. 


Walker stated, "This indicates that Parkinson's is neuroprotective as we age". However, when we increased Parkinson's disease expression everywhere, its beneficial effects increased by twice as much. 


He stated, "We were excited about this research from the beginning, but we did not know that the life span increase would be so impressive". 


An aged brain from a normal fly (left panel) and an age-matched brain with elevated neuronal park in levels (right panel) both contain clumps or aggregates of damaged proteins. As should be obvious, expanding park in levels in the maturing cerebrum lessens the collection of amassed proteins

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