End of Memory : Alzheimer's
Our memories make us who we are, where we belong and who are the people around us. We depend on our memories for thinking, learning and decision making. We interact with other people around us and make sense of the world, only through our memories.
When the destruction of the storehouse of our memories is complete because of Alzheimer’s disease, life and living no longer have meaning.
Even though I am not an expert on Alzheimer’s disease (AD), whenever memory is a topic for discussion, one can’t help but discuss AD. Over the years, my patients have asked me many questions about memory loss and Alzheimer’s dementia and in this article, I shall simply list those questions and try to answer them as I see it.
Q – Is weakening of memory that occurs with aging, any sign of AD?
A - Normally, with aging some weakening of memory occurs in every person. This is called, ”benign senescent forgetfulness”, scientific studies have shown that this has nothing to do with AD.
Q - Why then does ADs mostly occur in old age?
A – Aging is one of the biggest risk factors in AD which causes some circulatory, metabolic and cellular changes in our body, including our brain. Indeed, the risk of AD increases significantly with advanced age. For example, the studies have shown that the risk of AD is 3-4% at age 70; at age 80 the risk is 20%, and at age 90 the risk is 50%.
Q – What are the other risk factors for development of AD?
A – Type 2 diabetes is another important risk factor for AD. Blood glucose is readily available as a main source of energy for every organ in our body, especially for our muscles. As we age, our muscles become atrophic and our muscle mass is reduced. Yet we tend consume more glucose containing drinks, foods and our blood sugar levels start to go up. Our pancreas, in order to control blood sugar levels, increase its insulin output. But our cells with aging and metabolic changes have become insensitive to the effect of insulin, they can’t utilize glucose as before. We become insulin resistant, thus, our blood sugar and insulin levels become elevated. These changes in glucose metabolism seem to affect our brain cells, especially in the region of the hippocampus, in an adverse manner. Therefore, changing our eating habits, cutting down on simple sugars and deserts, remaining physically and mentally active, doing resistance exercises to reduce atrophy in our muscles becomes very important, to prevent the risk of late-onset AD.
The other important risk factor is, variation in lipo-protein regulatory gene, called a lipoprotein E (APOE). In cases of APOE4 variation, the blood cholesterol level cannot be properly regulated. This causes very high blood cholesterol levels and accelerated hardening of blood vessels (arteriosclerosis) and reduced blood circulation to our vital organs. Consequently, frequent strokes, TIAs (mini-strokes), heart attacks and ADs ensues. As a matter of fact, half of the late-onset of AD patients found to have AOPE4 gene variation. Cholesterol levels should be controlled by taking medications, diet and physical exercises.
The other risk factors are smoking, heavy drinking, obesity, sedentary life styles and environmental factors.
Q – How many types of Alzheimer’s disease are there?
A - Two types of ADs exist: Early-onset AD and Late-onset AD.
Q – What are the differences between these two types of AD?
A - Early-onset AD starts before age 50 and it is rapidly progressive. Genetic studies on these patients have shown that there is an inheritable gene defect in chromosome 21. Other scientists have shown the presence of additional gene defects (mutations) in protein synthesis coding genes. In this genetic disorder of AD, there is always a very strong family history of early-onset AD. Yet, in late-onset AD cases there is no family history, as seen in early-onset AD.
Q – What are the early clinical signs, and pathophysiological signs of AD?
A – Early clinical signs of AD is development of obvious defects, in recent memories. Sometimes it could be difficult to detect. Autopsy and histopathological studies on the brains of all types of AD patients have shown three defining characteristics of the disease:
1- The entire brain, especially the cortex of the brain is atrophic and shrunk.
2- There is a dense deposit of an abnormal paraprotein, called amyloid plaques, in the outside of the brain cells.
3- There is an accumulation of tangled proteins called, ”neurofibrillary tangles” in the inside of the brain cells.
Q – Is there any other form of dementia, besides ADs?
A – Yes there is, it is called “Frontotemporal Dementia-FTD”. Initially it was considered a part of AD. Its biological mechanism is the same as AD. The only difference is that misfolded proteins accumulate and kill the brain cells in frontotemporal region, not hippocampus as in AD. FTD is hereditary, starts in an early age, rapidly progressive, manifests itself with profoundly disordered social behaviors, language, reasoning and lack of control of impulses.
Q – Is there any treatments for AD?
A - Unfortunately no. But massive scientific studies continue to find the real reason for the formation and accumulation of amyloid plaques and tangled proteins in the brain cells. Once brain cells die, there is no regeneration or cure, prevention is the only option. Some recent scientific studies focused on preventing protein clamping by using antibodies that recognize and destroys these protein clamps .
