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Alzheimer’s disease

Definition

Alzheimer's disease (AD), one form of dementia, is a progressive, degenerative brain disease. It affects memory, thinking, and behavior.

Memory impairment is a necessary feature for the diagnosis of this or any type of dementia. Change in one of the following areas must also be present: language, decision-making ability, judgment, attention, and other areas of mental function and personality.

The rate of progression is different for each person. If AD develops rapidly, it is likely to continue to progress rapidly. If it has been slow to progress, it will likely continue on a slow course.

Alternative Names

Senile dementia/Alzheimer's type (SDAT)

Causes

The older you get, the greater your risk of developing AD, although it is not a part of normal aging. Family history is another common risk factor.

In addition to age and family history, risk factors for AD may include:

  • Longstanding high blood pressure
  • History of head trauma
  • High levels of homocysteine (a body chemical that contributes to chronic illnesses such as heart disease, depression, and possibly AD)
  • Female gender -- because women usually live longer than men, they are more likely to develop AD

There are two types of AD -- early onset and late onset. In early onset AD, symptoms first appear before age 60. Early onset AD is much less common, accounting for only 5-10% of cases. However, it tends to progress rapidly.

The cause of AD is not entirely known but is thought to include both genetic and environmental factors. A diagnosis of AD is made based on characteristic symptoms and by excluding other causes of dementia.

Prior theories regarding the accumulation of aluminum, lead, mercury, and other substances in the brain leading to AD have been disproved. The only way to know for certain that someone had AD is by microscopic examination of a sample of brain tissue after death.

The brain tissue shows "neurofibrillary tangles" (twisted fragments of protein within nerve cells that clog up the cell), "neuritic plaques" (abnormal clusters of dead and dying nerve cells, other brain cells, and protein), and "senile plaques" (areas where products of dying nerve cells have accumulated around protein). Although these changes occur to some extent in all brains with age, there are many more of them in the brains of people with AD.

The destruction of nerve cells (neurons) leads to a decrease in neurotransmitters (substances secreted by a neuron to send a message to another neuron). The correct balance of neurotransmitters is critical to the brain.

By causing both structural and chemical problems in the brain, AD appears to disconnect areas of the brain that normally work together.

About 10 percent of all people over 70 have significant memory problems and about half of those are due to AD. The number of people with AD doubles each decade past age 70. Having a close blood relative who developed AD increases your risk.

Early onset disease can run in families and involves autosomal dominant, inherited mutations that may be the cause of the disease. So far, three early onset genes have been identified.

Late onset AD, the most common form of the disease, develops in people 60 and older and is thought to be less likely to occur in families. Late onset AD may run in some families, but the role of genes is less direct and definitive. These genes may not cause the problem itself, but simply increase the likelihood of formation of plaques and tangles or other AD-related pathologies in the brain.

References

Rakel P. Conn’s Current Therapy 2005. 57th ed. Philadelphia, Pa: Saunders; 2005.

Moore DP, Jefferson JW. Handbook of Medical Psychiatry. 2nd ed. St. Louis, Mo: Mosby; 2004.

Goetz CG, Pappert EJ. Textbook of Clinical Neurology. 2nd ed. Philadelphia, Pa: Saunders; 2003.

Review Date: 2/13/2008
Reviewed By: Luc Jasmin, MD, PhD, Departments of Anatomy & Neurological Surgery, University of California, San Francisco, CA. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

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