There is a small but rich vein of science fiction (or alternate history now, take your pick) set at various times in a past couple of decades that might have been - had the look and feel of the 70s continued unabated, as though the decade never ended, and the world in fact worked the way it was thought to back then. One might look at Bug Jack Barron, for example, or some of Spinrad's other works.
This was brought to mind by Alexy Olovnikov and his "chronomeres," which I stumbled over today in their glorious entirety. While I'm sure this fellow is quite serious in his endeavors, plugging away at his theory in isolation and managing to make his way into serious journals, it has all the look and feel of an alternate history of aging science taken from a world in which the 70s never ended - and in which aging actually works the way it was thought to back then. A world in which growth hormone, pineal glands and lunar cycles mesh with DNA science, aging is a programmed phenonenon regulated at the level of organs rather than cells and molecules, and the discoveries of the 1990s and 2000s never happened.
As the basis for the lifelong clock and as a primary cause of aging, a process of shortening of hypothetical perichromosomal DNA structures termed chronomeres is proposed in the [central nervous system]. The lifelong clock is regulated by the shortening of chronomere DNA in postmitotic neurons of the hypothalamus. Shortening of these DNA sequences occurs in humans on a monthly basis through a lunasensory system and is controlled by release of growth hormone discharged from the anterior pituitary directly into the hypothalamus via local blood vessels. In adults, this process is under control of the pineal gland. It is further proposed that different forms of Alzheimer's disease (AD) are caused by somatic and inherited deletions of chronomeres followed by a further abnormally accelerated decrease in their activity, resulting in failures of neurotrophic and neuroendocrinal activities and in various cellular imbalances.
According to the redusome hypothesis, the aging of an organism is determined by the shortening of chronomeres (small perichromosomal linear DNA molecules). In this paper, a presumptive role for infradian hormonal rhythms is considered. Endogenous infradian rhythms are supposed to actively interact with those hormonal shifts which are governed by an exogenous infradian gravitational lunar rhythm. As a result of this interaction, the so-called T-rhythm is formed. Peaks of T-rhythms are used as the pacemaker signals to keep the life-long "clockwork" of the brain running. The "ticking" of this clock is realized by the periodically repeated shortening of chronomeres in postmitotic neuroendocrine cells, which occurs just at the maxima of T-rhythms. Shortening of telomeres in mitotic cells in vivo is a witness of the aging of the organism, but not the cause of aging. The primary cause of aging is shortening of chronomeres, the material carriers of a temporal program of development and aging. To recognize exogenous gravitational infradian rhythms, a special physiological system - the "lunasensor" system - evolved. It is assumed that it is a necessity to have a lunasensor as a particular variant of sensors of gravitation.
I'm rather hoping that second abstract above jumps out at you as absolutely alien to most of the aging science you've seen in the past few years. Here's an article from a few years back that's an easier read:
Early in the 70s of the 20th century, Russian researcher Alexy Olovnikov forecast existence of the chromosomes' end sequences - telomer, which shorten after each cell division. Aa lot of scientists believe now that telomere shortening leads to cell ageing. However, A.M. Olovnikov is convinced that telomer shortening is only the witness of ageing, and special DNA molecules - chronomeres - are responsible for ageing processes. Chronomeres are located in non-dividing cells of the cerebrum. So far, this is only a hypothesis based on the tremendous experimental material collected by Russian and foreign researches within the recent years.
It has to be said, this all triggers my crank sensors (and then some), for all that these papers appear in respected journals. Go hunt the scientific internet for signs of chronomeres and you'll meet with little but Olovnikov and the sound of crickets. A hypothetical component to the well-mapped cellular nucleus just isn't going to fly in this day and age, and the rest of it is all quite amazing - glands and hormones as giant controlling levers that can explain away aging. It seems like the aging science equivelant of building a working Babbage machine, or a computer constructed with miniaturized valve technology as it could be built today - a work of speculative art, but of little use to progress.
If you'd like to look at more modern and useful theories of aging, you might start with the Strategies for Engineered Negligible Senescence, which is built upon those theories with the best evidence and most active research communities behind them.