Alzheimer's Disease

Alzheimer's disease (AD) is the most common form of dementia in North America and currently afflicts more than four million people. Studies esti-mate that as many as five to ten percent of adults over the age of 65 will be affected. Over age 8o this figure can rise to one in three. Given the change in our population demographics towards longer life spans, this represents an enormous future burden. Alzheimer's disease follows heart disease, cancer and stroke as the fourth most common cause of death.

Alzheimer's is a neurodegenerative disease with progressive deterioration of memory, comprehension, intellectual function and behavior. It may have a subtle onset with a slow progression over twenty years or the patient may deteriorate rapidly with a devastating decline in mental capacity over a short period of time. The average duration is about seven years.

Not to be confused with the simple forgetfulness of normal aging, Alzheimer's leads to significant memory lapses, dramatic mood changes, emotional outbursts, childish behavior, inability to retain new information and general confusion or disorientation, particularly at night. Health and abilities decline until one is unable to care for oneself and eventually dies.

Alzheimer's disease is characterized by a degeneration of brain nerve cells and a shrinkage of brain mass. Although its exact cause has yet to be deter-mined, certain changes in the brain have been well identified. Patients have decreased or altered levels of certain neurotransmitters such as ACh and GABA which relay messages from neuron to neuron. Two other striking features are neurofibrillary tangles and neural plaque formation.

Several theories attempt to explain these changes. Alzheimer's was once thought to be a variant of the normal aging process. It used to be called `senile dementia.' It is now clear that Alzheimer's is an abnormal condition but that a number of factors may at least delay or slow its progression. Recent research has identified a blood protein called ApoE which appears to be altered in Alzheimer's patients and leads to nerve cell damage. Other studies point towards the interaction of this protein with heavy metals such as aluminum and mercury, and other elements such as iron, zinc and calcium, leading to plaque formation. A strong argument has been made for the role of oxidative stress and free radical formation in promoting the damage in these tissues.

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