Efficient, safe methods of gene therapy will be essential enabling technologies for the repair or obviation of several of the cellular and molecular lesions driving age-related disease and dysfunction. A recent paper from the Scripps Institute demonstrates a major step in this direction with the successful use of helper-dependent adenoviral vectors to rescue cells defective in lamin A, without detectable mutational side-effects.

At the third SENS conference, Dr. Samit Adhya of the Indian Institute of Chemical Biology presented a proof-of-principle for the use of an RNA import complex adapted from the parasite Leishmania to import arbitrary antisense RNA strands into mammalian mitochondria, reducing levels of a target protein by RNA interference. In a new study, Adhya’s group reports the successful use of the same technique to deliver mRNA sequences corresponding to proteins of the electron transfer chain, rescuing mitochondrial function in cells with mutations or deletions in those genes.

Much of the distraction in the literature of biogerontology, and an even higher ratio of studies cited and promoted in the popular media and the dietary supplement industry, derives from methodologically-poor lifespan studies in mice (or occasionally rats). In these studies, an increase in mean or maximal lifespan is reported, relative to short-lived controls, and claimed to be informative about the universal, degenerative aging process and the prospects for extending healthy life in humans living in the developed world.

The free radical theory of aging suggests that reactive oxygen species (ROS) and similar chemicals are responsible for a large part, or perhaps all, of the molecular and cellular damage that accumulates in aging bodies. However, more detailed analysis has revealed that some free radicals have essential signalling functions within the cell. These functions are likely to explain some of the failure of antioxidant therapy to extend lifespans in model organisms.

Beginning in the 1960s, a loose alliance led by social gerontologists but quickly coming to include biogerontologists, geriatricians, and patient advocacy groups successfully campaigned for a new understanding: that while some level of minor cognitive decline was indeed a “normal” and inevitable part of aging, the newly-rediscovered clinicopathological entity, “Alzheimer’s disease,” was exactly that: a disease, against which the full force of public and private biomedical research should be mobilized in the pursuit of a cure.