Last week, I posted on the topic of calorie restriction mimetics, with a focus on enhancement of autophagy and the operation of heat shock proteins as a path to extended longevity - or at least some repair of age-related cellular damage. Both autophagy and heat shock proteins contribute to cleaning up damage and dysfunctional molecular machinery in our cells, and are strongly implicated in the benefits to health and longevity provided by exercise and calorie restriction. As an addendum to that post, let me point out another example of early stage research into enhanced heat shock protein activity. This is an open access paper:
The misfolding of proteins into a toxic state contributes to a variety of neurodegenerative diseases such as Huntington, Alzheimer, and Parkinson disease. Although no known cure exists for these afflictions, many studies have shown that increasing the levels of protein chaperones [such as heat shock proteins], proteins that assist in the correct folding of other proteins, can suppress the neurotoxicity of the misfolded proteins. As such, increasing the cellular concentration of protein chaperones might serve as a powerful therapeutic approach in treating protein misfolding diseases.
Because the levels of protein chaperones in the cell are primarily controlled by the heat shock transcription factor 1 [HSF1], we have designed and implemented a pharmacological screen to identify small molecules that can promote human HSF1 activation and increase the expression of protein chaperones. Through these studies, we have identified HSF1A, a molecule capable of activating human HSF1, increasing the levels of protein chaperones and alleviating the toxicity of misfolded proteins in both cell culture as well as fruit fly models of neurodegenerative disease.
As a reminder, the FDA does not recognize aging as a disease and so will not approve therapies aimed at reversing biological consequences of aging that are present in everyone - such as the accumulation of aggregated metabolic byproducts and damaged proteins that could be (at least somewhat) attacked through boosted heat shock protein levels. Simple economics thus constrains research along these lines to treating the named diseases of aging or genetic diseases. The powerhouses of funding require profit at the end of the day, and there is no profit in therapies that are forbidden by regulators.
A wide range of scientific work that is presently constrained to development for late-stage named diseases might have some broader application for people suffering the effects of "normal aging" - but unless the present oppressive regulatory environment is overturned, the research and development required to explore that possibility will never happen.
Neef, D., Turski, M., & Thiele, D. (2010). Modulation of Heat Shock Transcription Factor 1 as a Therapeutic Target for Small Molecule Intervention in Neurodegenerative Disease PLoS Biology, 8 (1) DOI: 10.1371/journal.pbio.1000291