LONGECITY

http://www.abc.net.a.../11/2331197.htm

Notice this is from 11 august 08.
Did a search, but came up with noting related to this study, so just wanted to point it out and hear what you guy thought of it, and if you knew how it have progressed.

From the article:

Cuervo believes maintaining efficient protein clearance may improve longevity and function in all the body's tissues.

It is also possible that the same kind of "cellular clearance" can be achieved through diet, she says.

Research over the past decade has shown that restricted calorie intake in animals, including mammals, significantly enhances longevity.

"My ideal intervention in the future would be a better diet rather than a pill," she says.

This is actually the opposite of what I started doing -- raising my caloric intake and supplementing with whey protein in an effort to gain muscle mass...hope I am making the right choice. The result of the article seems very significant though. They stopped aging in a major organ, the liver. I wonder why the beneficial effects were only limited to the liver rather than the entire body?

uhh I think I am going to start a chocolate diet fat + carbs! (+ yummmmmmmmmmmm!!!!!!) and no proteins

This ties in with the existing large thread we have on autophagy. Please review that thread before posting to ensure we don't repeat anything that has already been discussed:

http://www.imminst.o...showtopic=24729

Fascinating, by increasing the number of copies of lysozyme receptor molecules, misfolded protein in older animals could be cleared at youthful rates.

( are you hearing this sens people? )

Fascinating, by increasing the number of copies of lysozyme receptor molecules, misfolded protein in older animals could be cleared at youthful rates.

( are you hearing this sens people? )

Rejuvepedia people (ok at this point only one person) are
Edited by caston, 04 March 2009 - 02:40 AM.

Go the Rejuvepedians!

Go the Rejuvepedians!

Indeed.



Mr Mox:

There was quite a bit of information about it posted on the geronotology research mailing list but you must subscribe first before you can search the archives.

Search for terms like liver, lysosome, Chaperone, Dr. Ana Maria Cuervo and so on.

Toxic proteins build up in organs over time

Researchers may have found a way to halt the biological clock which slows
down our bodies over the decades.

August 10, 2008; (BBC News) -- A New York team thinks it may have found the genetic
levers to help boost a system vital to cleaning up faulty proteins within our cells. The journal
Nature Medicine reported that the livers of genetically-altered older mice worked as well
as those in younger animals. They suggested it might one day help people with progressive
brain diseases.

[] These results show it's possible to correct this protein 'logjam' that occurs
in our cells as we get older, thereby perhaps helping us to enjoy healthier lives
well into old age. [] -- Dr. Ana Maria Cuervo; Yeshiva University

The researchers, from Yeshiva University in New York, are focusing on a process
which is central to the proper working of cells. The fundamental chemicals of cells - proteins -
often have very short working lives, and need to be cleared away and recycled as soon as possible.
The body has a system for doing just that, but it becomes progressively less efficient as we get
older. This leads to progressive falls in the function of major organs - the heart, liver and brain,
some of which contribute to the diseases of old age.

Dr Ana Maria Cuervo, from Yeshiva, created a mouse with two genetic alterations. The
first, when activated, boosted the number of specific cell receptors linked to this protein recycling
function, while the second allowed the first to be turned on whenever Dr. Cuervo wished simply
by modifying the animal's diet.

Switched On

She waited until the mice were six months old - the point at which age-related decline in the
protein-recycling system begins - then turned on the receptor gene. When examined at two years
old, the liver cells of these mice were far more effective at recycling protein compared with normal
mice. When the overall liver function of the very old genetically-modified mice was tested, they
performed at a comparable level to much younger mice. Dr. Cuervo said: "These results show it's
possible to correct this protein 'logjam' that occurs in our cells as we get older, thereby perhaps
helping us to enjoy healthier lives well into old age."

She now plans to test animal models of Alzheimer's and Parkinson's Diseases, believing that the
abnormal protein deposits in Alzheimer's in particular might be dealt with more effectively this way.
Thomas von Zglinicki, Professor of Cellular Gerontology at Newcastle University, said that the results
were "very exciting". "It's not often you see studies where they have managed to improve function in
this way. "What they seem to have managed is to maintain the mice at this young stage, and both
restore and maintain normal activity."

He said that it should, in theory, be possible to achieve the same effect across the whole body.
A spokesman for the Alzheimer's Society said: "As we age we have an increase in protein misfolding
and general faults in protein processing, so the ability to maintain an effective system to clear these
would be beneficial. "However, a direct line to the clearance of defective proteins in the brain is not
so clear from this research." _____________________________________________________________________________

Letter Abstract

Nature Medicine
Published On-line: August 10, 2008 | doi:10.1038/nm.1851

"Restoration of Chaperone-Mediated Autophagy in Aging
Liver Improves Cellular Maintenance and Hepatic Function"
by
Cong Zhang 1 & Ana Maria Cuervo 1

Abstract:

Chaperone-mediated autophagy (CMA), a selective mechanism for degradation of cytosolic proteins in
lysosomes, contributes to the removal of altered proteins as part of the cellular quality-control systems 1, 2.
We have previously found that CMA activity declines in aged organisms and have proposed that this
failure in cellular clearance could contribute to the accumulation of altered proteins, the abnormal cellular
homeostasis and, eventually, the functional-loss characteristic of aged organisms. To determine whether
these negative features of aging can be prevented by maintaining efficient autophagic activity until late
in life, in this work we have corrected the CMA defect in aged rodents. We have generated a double-transgenic
mouse model in which the amount of the lysosomal receptor for CMA, previously shown to decrease in
abundance with age 3, can be modulated. We have analyzed in this model the consequences of preventing
the age-dependent decrease in receptor abundance in aged rodents at the cellular and organ levels. We
show here that CMA activity is maintained until advanced ages if the decrease in the receptor abundance
is prevented and that preservation of autophagic activity is associated with lower intracellular accumulation
of damaged proteins, better ability to handle protein damage, and improved organ function.

Department of Developmental and Molecular Biology and Department of Anatomy and Structural Biology,
Marion Bessin Liver Research Center and Institute for Aging Research
1300 Morris Park Avenue
Albert Einstein College of Medicine
Bronx, NY 10461; USA

Edited by caston, 05 March 2009 - 08:08 AM.