Many of you have asked about Helen Blau’s work at Stanford, using telomerase mRNA [FASEB Journal]. Helen sent me a copy of her article when it came out and I’m a serious fan of her work. As some of you know from my upcoming book, The Telomerase Revolution, there are four approaches to resetting telomeres: […]
Four Ways to Lengthen Telomeres
Many of you have asked about Helen Blau’s work at Stanford, using telomerase mRNA [FASEB Journal]. Helen sent me a copy of her article when it came out and I’m a serious fan of her work. As some of you know from my upcoming book, The Telomerase Revolution, there are four approaches to resetting telomeres: 1) put in a new telomerase gene, 2) activate the telomerase gene that is already in cells, 3) put in the mRNA (as Helen’s group did) for telomerase, or 4) put in the telomerase protein itself.
The first problem with mRNA is that the molecule is incredibly fragile and has a short half-life at body temperature, making it hard to work with in the lab (in vitro) and even harder to work with in patients (in vivo). The second problem (with both mRNA and protein) is that you only get one copy of the final telomerase enzyme, whereas if you put in the gene or activate the gene, you get multiple copies of the enzyme and a lot more “bang for your buck”. In short, mRNA is great, but has a low ROI, clinically speaking. The third problem, a recurrent one in this field, is that if you read either Helen’s paper or the slew of media articles and interviews since publication, the emphasis is always on treating “genetic disease” (such as one of the muscular dystrophies) rather than “aging disease” (such as Alzheimer’s). There is an unspoken and almost universal assumption that genetic diseases like the various muscular dystrophies are “real”, but aging diseases like Alzheimer’s aren’t true “diseases” at all, but they “just happen because things wear out”. This common assumption leads most researchers to focus on inherited genetic conditions exclusively and completely ignore normal aging processes and their associated clinical pathology – such as Alzheimer’s. Even when researchers DO focus on Alzheimer’s they operate on the assumption that it must involve a “bad gene” (such as APOE4).
Both assumptions are false, but are shared by most of the academic and medical research community, even if neither assumption is ever clearly stated or acknowledged. Since researchers “know” that aging is not a classic genetic disease, they are equally complacent in thinking that aging diseases cannot be treated by a genetic approach. The result is that almost no one approaches aging diseases in a practical way, using fundamental interventions such as telomerase mRNA, telomerase activation, telomerase protein, or – as in our case at Telocyte – telomerase gene therapy.