A new theory on the control of aging

I have long believed that we don’t wear out but are turned off after a certain age is reached. One tragic example is the genetic disease Progeria where children age prematurely due to a defect in their lamin gene that results in the reduced ability of stem cells to carry out normal and continuous tissue regeneration that keeps us young during part of our life. Progeria shows that without this regeneration we would all age much more rapidly like so many other animals.

Another mechanism has also come to light in recent years. This is the effect of micro inhibitory RNAs which are defined below from http://en.wikipedia.org/ . Only a few percent of our genome actually codes for proteins, these RNA molecules are coded by some of the so-called “junk” DNA segments.

In genetics, microRNAs (miRNA) are single-stranded RNA molecules of about 21-23 nucleotides in length, which regulate gene expression. miRNAs are encoded by genes that are transcribed from DNA but not translated into protein (non-coding RNA); instead they are processed from primary transcripts known as pri-miRNA to short stem-loop structures called pre-miRNA and finally to functional miRNA. Mature miRNA molecules are partially complementary to one or more messenger RNA (mRNA) molecules, and their main function is to downregulate gene expression. They were first described in 1993 by Lee and colleagues in the Victor Ambros lab ^[1], yet the term microRNA was only introduced in 2001 in a set of three articles in Science (26 October 2001).^[2]

^{Picture of a microRNA precursor that is shortened eventually to the 21-23 nucleotide form.:}

Euenia Wang of the University of Louisville has recently published:

In general microRNAs, while themselves not coding for any protein product, negatively regulate the expression of target genes by either degrading their message or inhibiting translation by binding to their 3'-untranslated region (UTR). Thus, possible derailment of these negative regulators for gene expression in mid-life may be the putative force inducing molecular frailty in individual cell signaling, and in time leading to tissue-wide dysfunction. A challenge for future research is then to identify these dysfunctional microRNAs, in order to develop advance diagnosis and therapy to combat mid-life decline, a preventive medicine approach to block, delay or reduce the risk of old-age diseases.