Alzheimer’s Disease and Mitochondrial Dysfunction: A Path to Prevention By Debra Gibson, N.D.
ike cancer, Alzheimer’s Disease (AD), the most common form of dementia, is a health issue with a larger-than-life persona. The feelings of fear and helplessness it inspires are understand- able in light of the limited knowledge of its origins, the ineffective- ness of treatment options offering long-term benefit, and the progres- sive, devastating nature of the disease.
L Who is Vulnerable, and Why
As the baby boomer population ages in the coming decades, increasing numbers of Alzheimer’s diagnoses are projected; even now it affects one in eight Americans over age 65, and about half of those age 85 and older have this eventually fatal disease. Yet while advancing age is the greatest risk factor, the development of Alzheimer’s disease is not a normal part of aging. Determining who is vulnerable and why is key to discovering pathways to prevention. Although the causes of the disease are currently unknown (except in the fewer-than-one-percent who have the purely genetic form of the disease), a number of risk factors have been identified which can be minimized or even eliminated through changes in lifestyle, environ- mental exposure and nutrition, thereby reducing the possibility of developing AD later in life.
A New View of Alzheimer’s Disease In addition to the gradual loss of memory associated with
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AD, other common manifestations include alterations in behavior and mood, confusion, disorientation and impaired judgment, and gradual loss of the ability to perform basic functions of living. The course of AD, based on criteria issued in 1984, has been thought of as having three stages: an early mild form; a mid-stage moderately symptomatic form; and the late stage severe form of the disease. New guidelines presented in 2011 by the Alzheimer’s Associa- tion and the National Institute on Aging, however, demonstrate an important change in perspective on AD. These new criteria recog- nize that changes in brain function occur as many as twenty years before the onset of mild dementia, and propose a very different three-stage model for AD: a preclinical stage, in which no symptoms exist but identifiable changes have occurred in the brain; a second phase, called mild cognitive impairment (MCI), in which significant and noticeable problems in thinking or memory are occurring, but these problems don’t interfere with the person’s ability to function; and the third stage, Alzheimer’s dementia, which includes all three stages of the older guidelines (mild/moderate/severe impairment of brain function). These new guidelines for AD imply that there exists a continuum for its development and progression, beginning decades before the disease is diagnosed. While this idea may be disturbing for those who have the occasional senior moment, it contains seeds of hope for prevention of this justifiably dreaded condition, because even in people diagnosed with MCI (second stage in the new guide- lines), many do not progress to dementia, and some recover normal brain function. Although the reasons for these reversals of brain cell changes are not understood, the fact that they occur is significant, for it represents an avenue for prevention, even in those clearly at risk for AD.
What We Know For Sure about Alzheimer’s If Alzheimer’s disease is not a normal consequence of aging,
then what causes some brains to get sick, atrophy and die, and oth- ers to function well throughout life? Evidence points to a multifactorial cause for AD, meaning that a number and variety of contributory factors, which may differ from individual to individual, act together over time to destroy brain
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