Some New Longevity Discoveries

 

Scientists Discover Common Antibiotic Can Slow Aging

 Animals given Doxycyclin throughout life lived longer

A multinational group of scientists have discovered a key mitochondrial pathway invloved in lifespan can be manipulated by exposure to a common drug at key life stages.

The study began by studying gene transcription variability among mice of different eventual life spans capitalising on the natural variability to find genes linked to longevity.  They discovered a group of three genes on chromosome two that had never previously been  linked to lifespan.  It was found decreased expression of these genes correlated with longer lifespan.

The genes were shown to code for mitochondrial ribosomal proteins (MRP) which act to make protein from mitochondrial DNA within the mitochondria.

It turns out that when MRP levels are reduced, the stress of protein imbalance within the mitochondria causes  a reaction called in the unfolded protein reposnse.  When the unfolded protein response was made to occur at specific developmental stages, the animals lived longer.

Furthermore the group showed this mechanism was so important as to be conserved from worms to mammals - inhibiting MRP in worms prolonged their lifespan too.

Pharmacological inhibition of MRP with certain drugs also were able to prolong lifespan, when given to young animals.  The scientists used the antibiotic Doxycyclin as mitochondria are evolutionarily derived from bacteria that became part of animal cells.  Animals given doxycyclin throughout life lived longer.  Cellular studies also proved the antibiotic reduced mitochondrial respiration in mammalian cells.

They conclude:

The apparent conservation of mitonuclear protein imbalance and UPRmt as a general longevity mechanism should invite further studies to explore whether targeting UPRmt can prevent ageing associated functional decline and treat diseases linked with ageing

Boosting Single Gene Found to Increase Maximum Lifespan 28%

20 days ago by Lyle J. Dennis, M.D. 3

Scientists at UCLA have discovered that increased expression of a single gene increases the lifespan of fruitflies by more than 25%.

The gene is called Parkin, and when defective is implicated in the development of Parkinson’s disease.

The gene normally functions to recycle cell proteins and defective mitochondria.  It acts to tag defective structures so they are degraded an recycled.  It tags them by adding a ubuquitin to the protein’s surface.

It seems clear that at least in part, aging is due both to accumulation of damaged and misfolded proteins in the cell, and increasing numbers of defective and leaky mitochondria, the latter of which release reactive oxygen species which then lead to further damage.

So it seems plausible that if it were possible to amplify the functioning of the cellular garbage disposal system, aging might be reduced.

Amazingly this is just what was found.

When parkin was genetically overexpressed in all cells of fruitfiles they exhibited a dramatic 28% increase both in mean and more importantly maximum lifespan.  In addition these long lived flies showed no loss of function and appeared healthy.

The authors conclude:

Our work strongly suggests that treatments designed to augment Parkin expression during aging may delay the onset and progression of a number of age-onset diseases

Of course we cannot genetically modify adult humans, however the development of small molecules which can either activate, enhance or mimic Parkin within cells could lead to dramatic increases in healthy human lifespan.

from http://extremelongevity.net