A Modest Gain in Mouse Lifespan via Pharmacological Means of CISD2 Upregulation

The usual progression of ways to tinker with metabolism in order to affect the pace of aging is much as follows: (a) identify an interesting mechanism associated with a single gene; (b) create mouse lineages in which the expression of this gene is manipulated in a controlled way via genetic engineering, to observe the outcomes; (c) use some form of gene therapy to overexpress or knock down that gene in mice, and note differences in life span and manifestations of aging; (d) search the drug databases for small molecules that might affect expression of the gene of interest without causing too many undesirable side-effects; (e) produce animal studies to show that the small molecule approach produces the same outcome as the genetic studies, but to a smaller degree. If further development is then undertaken, it typically picks up from the small molecule demonstration, which is almost always unimpressive in comparison to the gene therapy. The economics of development still heavily favor working with small molecules, however, to the point at which producing a marginal therapy that is less likely to help patients is an acceptable cost of doing business. This is particularly the case since early investors typically make their returns, and are on to the next project, well before the issues associated with marginal effect sizes arise in phase II or phase III clinical trials. It is a broken system, and the obvious fix, that most small molecule development should in fact be gene t...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs