At the moment, there are four companies planning human trials to reset telomeres using telomerase genes. In every case, the intent is to put the telomerase genes (hTERT and hTERC) into human patients in an effort to cure age-related diseases. Let’s look at the diseases and then the companies involved. Essentially, all age-related diseases occur […]
Biotech and Alzheimer’s
At the moment, there are four companies planning human trials to reset telomeres using telomerase genes. In every case, the intent is to put the telomerase genes (hTERT and hTERC) into human patients in an effort to cure age-related diseases. Let’s look at the diseases and then the companies involved.
Essentially, all age-related diseases occur because of cell aging. In the cases of osteoarthritis (chondrocytes) and osteoporosis (osteoblasts and osteoclasts), this process is straightforward. In the case of heart disease, it’s a bit more complex: the heart cells don’t die because they age, but because the arterial cells age. The endothelial cells, that line your coronary arteries for example, divide, loose telomere length, alter their gene expression (which is the key to the whole cellular pathology), and become dysfunctional. The result is gross changes in the wall of the artery: cholesterol plaques, inflammation, mast cells, foam cells, and general histological mayhem. And when the artery gets clogged, or when clots break off, the heart (and other organs) pay the price. In the case of a heart attack, the heart is the innocent bystander, whose cells die not because they age, but because of the pathology in the vessels that supply them. Much the same occurs — indirect aging — in neurodegenerative diseases such as Alzheimer’s disease. The innocent bystander is the neuron, that neither divides nor ages, but which is critically dependent upon the surrounding cells, especially the microglial cells. These cells, responsible for metabolically supporting the neurons and clearing beta amyloid, for example, show the initial aging changes. Their telomeres shorten , their gene expression changes, and they no longer clear beta amyloid as well. This process — “microglial activation” — is the initial step in Alzheimer’s dementia and — like all other age-related disease — is ultimately the result of cell aging.
As we finally begin to understand age-related disease and the cell aging that causes it, we are faced with the obvious question. Can we reverse the process? At present, medical therapy has no way of altering the underlying disease processes of any age-related disease, whether osteoarthritis, osteoporosis, atherosclerosis, Alzheimer’s disease, or any other common aging condition. But what if we could reset gene expression, reset the epigenetic pattern to that of young cells? We’ve known that we could do exactly that — in the lab — since 1999, but can we do it in humans? A number of studies have shown we can do exactly that in mice and rats, particularly in Maria Blasco’s lab in Madrid, but what about human patients? How long must we wait to cure Alzheimer’s disease?
At present, there is a small Canadian company that has failed to “gel” (or get financing), a new biotech group in Seattle that intends to go “offshore” (if they can get financing), and two linked companies that intend to progress to human trials as rapidly as possible. These latter two consist of a US-based biotech company (Telocyte) and a sister organization (non-profit) in the UK. Telocyte is aimed directly — and solely — at curing Alzheimer’s disease.
Telocyte sees no reason to wait, nor should you.