A fraction of the damage of aging is caused by the build-up of biochemical waste within and between our cells. Some is common to all of us and a byproduct of the normal operation of metabolism, such as the amyloid implicated in Alzheimer's, which can be found in small amounts even in the young, or lipofuscin that increasingly harms our lysosomes. Other types of biochemical waste are peculiar to those unfortunate enought to suffer particular forms of genetic damage - such as the mutation that causes Huntington's disease.
It is instructive to watch early research and progress in treating diseases where the damage done depends upon a build up of unwanted proteins. Some of the lessons learned and new technologies deployed could be turned to address other types of biochemical, ones whose buildup contributes to the aging process. Here's an example of what I mean:
A new study has identified a potential strategy for removing the abnormal protein that causes Huntington's disease (HD) from brain cells, which could slow the progression of the devastating neurological disorder. [Research describe] how an alteration to the mutated form of the huntingtin protein appears to accelerate its breakdown and removal through normal cellular processes.
A key observation was that [the method used], while increasing the removal of mutant huntingtin, had little effect on the normal version of the protein. "One of the major challenges of research into neurodegenerative disorders like Huntington's, Alzheimer's and Parkinson's diseases - all of which involve accumulation of proteins within the brain - has been how to activate degradation machinery that only removes the disease-causing proteins and leaves normal proteins untouched."
As the ability of researchers to manipulate the elements of human biochemistry grows, we should expect to see ever more opportunties to harness and redirect existing cellular capabilities as a part of a new therapy.