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Biology 202, Spring 2005
Second Web Papers
On Serendip

Alzheimer's Disease

Erin Deterding

One of the most common diseases of aging is Alzheimer's disease. This debilitating disease of neuronal degeneration affects about five million Americans, and is one of the most crippling of age-related illnesses (1). With so many elderly people affected, it's important to understand what Alzheimer's is, what causes it, and what is being done to prevent the effects of this seemingly inescapable sickness.

The classic symptoms of Alzheimer's disease all affect cognitive functioning, but range in their severity (2). For example, those exhibiting early signs of Alzheimer's may find themselves with slight memory loss, while those in the advanced stages have trouble with thinking and perception (3). With such debilitating degeneration to cognitive functioning, Alzheimer's is the leading cause of dementia among the elderly (1).

One of the most interesting aspects of Alzheimer's disease is how the brain is changed throughout the course of the disease. While it is still not completely understood, there are a few key abnormalities that are thought to be the cause of Alzheimer's.

The first of these abnormalities occurs in a specific protein called amyloid precursor protein (2). This protein is found spanning cells in the brain, and is usually spliced so that portions remain inside and outside of the cells. If spliced incorrectly, a protein called beta-amyloid can be formed (4). Beta-amyloid is precursor to the characteristic plaque build-up found in the brains of those suffering from Alzheimer's disease (4). These plaques are comprised of a beta-amyloid core surrounded by clumps of dying axons and dendrites (2). Plaques can ultimately cause swelling of axons, making it impossible for information to be conducted from one neuron to the next, thus causing the deficits in cognitive function (5).

One of the first systems to be affected by Alzheimers is the acetylcholinergic system. These neurons are found in subcorticol areas, such as the nucleus basalis found in the basal forebrain, and in the hippocampus and medial septum (6). Because acetylcholine is an important neurotransmitter for learning and memory, it is thought that the loss of such neurons is the cause for early memory loss in Alzheimer's patients (6).

In addition to plaques, another characteristic change in the brains of patients with Alzheimer's are a build up of neurofibrillary tangles. In these tangles, another protein, tau, hyperphosphorylates fibers inside the cells, causing them to become tangled together. The combination of these extracellular plaques and intracellular tangles is thought to be the leading cause of the neuronal death that leads to Alzheimer's disease (2).

While the causes of Alzheimer's are thought to be partly due to environmental aspects, the biological aspect of the disease is becoming better understood. Research indicates that there may be specific genes that can increase the risk of developing Alzheimer's (7). An understanding of how these genes affect the onset of Alzheimer's may help researchers discover a way to slow down or stop the progression of the disease.

Some recent discoveries in the research of Alzheimer's have shed some light on this intricate disease. One such discovery has shown that cannabinoid brain receptors may play a role in decreasing inflammation in the brain caused by Alzheimer's. Patients with the disease have been shown to have decreased functioning of these receptors, indicating that they do not fully benefit from the protective factors of the cannabinoid receptors (8).

In addition, research has shown that the effects of beta-amyloid on the brain can be reversible due to an anti-amyloid antibody. This discovery points to the persistence of beta-amyloid plaques as a cause of the deficits seen with Alzheimers. However, the study also indicates that this persistence may not be permanent (9).

More and more information concerning Alzheimer's disease seems to be discovered everyday; however, there is still no cure (3). It seems that while the research is continually making sense of more complex issues regarding the onset and progression of the disease, there is still much to be learned. For example, what are the implications of interactions between genes and splicing mutation of amyloid precursor protein? Is the splicing error an isolated incident, or do the genes associated with Alzheimer's control for those errors? Another important question is what are all the structures in the brain that are affected by the disease? While ultimate result of Alzheimer's is shrinking of the brain, does that mean that all parts of the brain are directly involved in the disease, or is the entire brain affected as a secondary side effect (2)? These questions may some day be answered, but for now, they remain a mystery.


1)Alzheimer's Disease: Understanding Alzheimer's, The Alzheimer's Information Site.

2)Meyer, J.S. and Quenzer, L.F. Psychopharmacology: Drugs, The Brain, and Behavior. Massachusetts: Sinauer Associates, Inc, 2005. 148-149.

3)Treatment, The Alzheimer's Information Site.

4)About Drugs Targeting Beta-amyloid, and the "amyloid hypothesis", Alzheimer's Association Website.

5)Nerve 'Traffic Jam' Marks Early Alzheimer's, The Alzheimer's Information Site.

6)Carlson, N.R. Physiology of Behavior, 7th Edition. Boston: Allyn and Bacon,2001. 448.

7)Doctors Identify Possible New 'Alzheimer's Gene, The Alzheimer's Information Site.

8)Marijuana-like Ingredient Could Slow Alzheimer's, MSN Health & Fitness Website.

9)Antibody Helps Reverse Alzheimer's Nerve Damage, MSN Health and Fitness Website.

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