This piece from Discover is a fascinating look into why we age. It has a direct relation to Alzheimer’s disease:
In recent years, gerontologists have overturned much of the conventional wisdom about getting old. Aging is not the simple result of the passage of time. According to a provocative new view, it is actually something our own bodies create, a side effect of the essential inflammatory system that protects us against infectious disease. As we fight off invaders, we inflict massive collateral damage on ourselves, poisoning our own organs and breaking down our own tissues. We are our own worst enemy….
When you start to think about aging as a consequence of inflammation, as Tracy and many prominent gerontologists now do, you start to see old age in a different, much more hopeful light. If decrepitude is driven by an overactive immune system, then it is treatable. And if many chronic diseases share this underlying cause, they might all be remedied in a similar way. The right anti-inflammatory drug could be a panacea, treating diabetes, dementia, heart disease, and even cancer. Such a wonder drug might allow us to live longer, but more to the point, it would almost surely allow us to live better, increasing the odds that we could all spend our old age feeling like Jim Hammond: healthy, vibrant, and vital. And unlike science fiction visions of an immortality pill, a successful anti-inflammatory treatment could actually happen within our lifetime.
The ‘Tracy’ referred to in the article is Russell Tracy, a professor of pathology and biochemistry at the University of Vermont College of Medicine. By and large, treating aging in this way is science fictional at the present time, but it shows how research into aging could eventually lead to new Alzheimer’s treatment. The article goes on: “The evidence that inflammation is behind other diseases is indirect, but it is mounting. Researchers have long known that in patients with Alzheimer’s, the areas of the human brain clogged with senility-associated plaques also bristle with inflammatory cells and cytokines.”
In short, Alzheimer’s is potentially an immune response due to aging: “Several years ago some neuroscientists began to suspect that immune cells in the brain, in their efforts to destroy the plaques, might release poisons and inadvertently harm neighboring, healthy brain cells.”
Cure the way the body undergoes this immune response and you’ll have a potential cure for Alzheimer’s. Still, this may not be the smoking gun, as there is some amount of confusion as to why some aging brains develop Alzheimer’s and some do not.
Neuropathological examination can detect occasional individuals in whom the microscopic features typical of late-onset Alzheimer’s disease are present yet a clinical history of dementia is absent. On other occasions, the converse seems true: individuals seriously disabled in life by dementia show at death only mild pathological features of Alzheimer’s disease.
There are many things we clearly do not fully understand. The immune response issue isn’t the whole picture either, and there are cases where people with amyloid plaque build-up do not always develop the disease. Alzheimer’s disease is a fundamentally complicated disease and amyloid plaque may be more of a guidepost than a smoking gun for curing it. There is still a lot to be discovered both about immune response and why this response may trigger Alzheimer’s in some but not others.
Gene Research
Nevertheless, research on aging could be a vital component to finding ways to diagnose and cure Alzheimer’s. Promising genetic research into aging has led to developments in treating AD. A new study released in the July 23rd issue of Cell connects a gene linked to aging and possible Alzheimer’s treatment:
The researchers found that SIRT1 appears to control production of the devastating protein fragments, termed A-beta peptides, that make up amyloid plaques. They also showed that in mice engineered to develop Alzheimer’s plaques and symptoms, learning and memory deficits were improved when SIRT1 was overproduced in the brain, and exacerbated when SIRT1 was deleted.
People worried about developing Alzheimer’s disease aren’t necessarily interested in the proverbial fountain of youth – they just want to find a way to curb the disease, regardless of halting the overall aging process. While “halting the aging process” may sound like a fantastical and impossible idea, research into aging is still a major component of Alzheimer’s disease research. Though a true fountain of youth that extends lifespan many years may come well after the discovery of a cure for Alzheimer’s disease, the research into the former may very well be the thing to spark the latter.
Technorati Tags: Aging, autoimmune disorders, Cell Magazine, genetic variants, neuroscience
Related posts
Aricept (donepezil HCl), is a prescription medicine used to treat the three stages (mild, moderate and severe) of Alzheimer’s disease. Based on the FDA announcement, patients suffering from mild Alzheimer’s can continue to take the conventional lower dose (up to 10 mg/day), while those suffering from moderate to severe Alzheimer’s can take the new dose of up to 23 mg/day. Aricept alleviates the symptoms of Alzheimer’s – and (although not proven) there have been some reports of improvement in cognition and behavior.
The FDA approval came as a result of a study of 1,467 patients with moderate to severe Alzheimer’s who were tested after both dosage levels (10mg/day and 23 mg/day). Patients are generally started on a much lower dose of 5 mg/day before ramping up to 10 mg/day after 4-6 weeks. The higher dose of the drug is only available to patients who have been taking Aricept’s lower dose of 10 mg/day for at least 3 months.