Scientists are studying changes of gene inactivation as our muscles age. Useful information for understanding the arrows of causation between genetic changes and other changes in cells as they age.
Our epigenome is a set of chemical switches that turn parts of our genome off and on at strategic times and locations. These switches help alter the way our cells act and are impacted by environmental factors including diet, exercise and stress. Research at the Buck Institute reveals that aging also effects the epigenome in human skeletal muscle. The study, appearing on line in Aging Cell, provides a method to study sarcopenia, the degenerative loss of muscle mass that begins in middle age.
The results came from the first genome-wide DNA methylation study in disease-free individuals. DNA methylation involves the addition of a methyl group to the DNA and is involved in a particular layer of epigenetic regulation and genome maintenance. In this study researchers compared DNA methylation in samples of skeletal muscle taken from healthy young (18 - 27 years of age) and older (68 – 89 years of age) males. Buck faculty and lead scientist Simon Melov, PhD, said researchers looked at more than 480,000 sites throughout the genome. "We identified a suite of epigenetic markers that completely separated the younger from the older individuals – there was a change in the epigenetic fingerprint," said Melov. "Our findings were statistically significant; the chances of that happening are infinitesimal."
A very thorough understanding of genetic regulatory changes in aging will tell us whether gene therapy or drugs to alter gene expression could help rejuvenate muscle. Will we find no effective solution for muscle aging short of cell therapy?
Looks like some of the problems with muscle aging might be due to degradation mechanisms for muscles to receive signals from nerves.
Melov said scientists identified about six-thousand sites throughout the genome that were differentially methylated with age and that some of those sites are associated with genes that regulate activity at the neuromuscular junction which connects the nervous system to our muscles. "It's long been suspected that atrophy at this junction is a weak link in sarcopenia, the loss of muscle mass we get with age," said Melov. "Maybe this differential methylation causes it. We don't know."
How much of the methylation is just random bad stuff happening to the cell? How much of it is intentional in order to shut down genetic systems that are too damaged to still function? Even if the methylation patterns with age are not needed for protection that does not mean we'll necessarily be able to find ways to reverse them. It might be easier to send in cell therapy regardless of why the epigenomic state of cells increasingly hobbles their function with age.
|Share |||Randall Parker, 2013 November 24 08:52 PM|