ALZHEIMER'S DISEASE [ back to Glossary Index ]
Alzheimer's Disease is a degenerative disorder of the brain first described in 1906 by German neuropathologist Alois Alzheimer, and named after him. On a structural level it is characterized initially by the appearance of senile plaques (deposits of sticky protein called beta-amyloid which clog brain cells) followed by development of neurofibrillary tangles (extravagant overgrowth of axons which form dense, twisted clusters) in the dying cells. The process ends with the with the death of neurons in the hippocampus (where short term memory is processed) and in the basal ganglia where much of the brain's supply of acetylcholine is produced (the Nucleus Basilas of Meynert). Abnormal levels of amyloid in the brain are directly associated with cognitive decline. Current research indicates that beta amyloid accumulation triggers activity by scavenger cells in the brain called microglia, which pump out toxic immune compounds that go too far by destroying the brain cells harboring the beta amyloid.

Functionally, the Alzheimer's patient loses short term and long term memory capacity, and suffers greatly from confusion, disorientation and depression. AD patients forget their own intentions, wander off and can become aggressive. They show increasingly poor judgment as the disease progresses. It is estimated that there are 4 million Americans with AD right now, and that the numbers will grow astronomically as Baby Boomers age. Current estimates are that 14 million people will die of AD between 2000 and 2025. On a rare basis it can afflict people in their 40s or 50s but is much more common in older people. Experts estimate that 5-10% of people between 65-75 years of age have it, about 35% between age 75-85 and that 50% of people over than 85 have it. An important risk factor is the presence of the APOE-e4 gene. Recent research at Washington University Medical School by Dr. David Holtzman and a team from Eli Lilly and Company has shown that in the presence of this gene, beta amyloid will accumulate abnormally into plaques which clog and kill neurons. Research done in the 1990s showed that people with poorer outcomes following a TBI than people of similar circumstances frequently had the APOE-e4 gene, giving rise to the supposition that TBI could precipitate Alzheimer's Disease in persons with that gene. High intake of "bad fats" (the Omega 6 fatty acids which increase LDL cholesterol) has been associated with increase in amyloid and onset of AD (see our section on The Brain and Nutrition)

Current treatment involves drugs which boost the supply of acetylcholine in the brain, anti-depressants and behavioral therapies which include showing AD patients videos of their life history. AD has recently become a concern of people who suffer a Traumatic Brain Injury (TBI), because of studies showing increased risk of AD following a TBI. However, the studies show a significant increase in the risk of AD only for the small subgroup of TBI patients who have the APOE-e4 allele for AD.  This year scientists at SmithKline Beecham identified the enzyme which unzips the beta-amyloid peptide from a longer precursor protein. It is anticipated they will find a way to block the action of that enzyme and slow the build up of beta amyloid deposits in the brain. Whether this will prevent AD, slow the progression of AD or reverse it, is not known, because scientists are still debating whether the amyloid plaques are a cause or an effect of AD. Currently the most widely held hypothesis is that accumulation of beta-amyloid is the crucial first step in the gradual death of brain cells, but that the death of brain cells is caused later by activation of caspase enzymes, accumulation of tau protein in axonal tangles and/or other factors not yet known.