I confess that I’ve yet to find time to continue through each of several age-related diseases. In partial recompense, let me offer the following, which is adapted from the quarterly newsletter that I put out for Telocyte. While it focuses on Alzheimer’s disease, the import is generic, applying to all age-related diseases. How Alzheimer’s works […]
Aging Disease, Aging, and Alzheimer’s
- beta amyloid
- Curing Alzheimer's
- tau protein
- Vascular dementia
I confess that I’ve yet to find time to continue through each of several age-related diseases. In partial recompense, let me offer the following, which is adapted from the quarterly newsletter that I put out for Telocyte. While it focuses on Alzheimer’s disease, the import is generic, applying to all age-related diseases.
How Alzheimer’s works
Why do we get Alzheimer’s or any other dementia? And why do some of us get it so early, while others do not? What causes Alzheimer’s and other dementias?
Alzheimer’s occurs when the neurons of the brain become dysfunctional and are lost. The neurons, however, depend upon the health and function of the surrounding glial cells, cells that take care of the metabolic and physiological needs of those critical neurons. In some sense, the neurons are merely the “innocent bystanders” as the glial cells fail. In all of the various types of Alzheimer’s dementia (sporadic, familial, etc.) and indeed in all of the age-related dementias (Lewy Body, Frontotemporal, Parkinson’s, etc.) it is the glial cells that are the single common denominator. The glial cells fail as, having divided repeatedly over your lifetime, their telomeres shorten, and their pattern of gene expression becomes abnormal, insufficient, and pathological. The process is remarkably complex and affects a myriad of processes – including beta amyloid and tau tangles – but the fact that telomere shortening is always central to the pathology is what allows us to target telomeres in our goal of curing and preventing Alzheimer’s and other age-related dementias.
Yet we know that a number of variables seem to play a role in the onset of Alzheimer’s disease. One person shows symptoms at age 50, another at age 80. One person, with a history of head injuries (e.g., football players), or a history of infections, or a history of chemotherapy, comes down with a dementia far earlier than another person. Not only does age itself play a role, but so do our genes (e.g., a double ApoE4 allele), and your life-long medical history. Why do so many things appear to play a role in our risk of dementia? The reason is that these are variables that accelerate glial cell loss and replacement, thereby accelerating aging and age-related disease. The result is dementia. Upstream, we have all the various risk factors – each of which determines the rate at which our glial cells divide and age – and downstream we have all the classic findings of dementia – including beta amyloid plaques, tau tangles, and a host of other findings.
The one oddball, perhaps, is vascular dementia, but even here we find that there are cells that show the same process of telomere shortening and cell failure. In the case of vascular dementia, the problem lies not with the glial cells, but the cells that line the blood vessels of the brain: the vascular endothelial cells. While the cells are different – glial or endothelial cells – the outcome is the same: the cells divide, telomeres shorten, gene expression changes, the cells cease to work normally, and the result is the failure and death of neurons. More importantly, the result is the loss of those we love.
In all cases, however, whatever the type of dementia, the key is that we can prevent or cure such dementias not by dealing with the dozens of risk factors that lie upstream, nor by trying to repair the dozens of findings that lie downstream, but by intervening in a single, critical point: the telomere.