Alzheimer's Disease currently affects more than four million Americans. Alzheimer's is a disease characterized by the progressive degeneration of areas within the brain, resulting in cognitive and physical decline that will eventually lead to death. It is important to emphasize that Alzheimer's disease (AD) is not a normal part of aging. Although AD typically appears in those over sixty-five, it is a neurodegenerative disease, quite distinct from any aging-related cognitive decline. Because Alzheimer's is eventually fatal, and because the decline typical of an Alzheimer's patient is so devastating, much research is currently being done to investigate potential treatments. With the elderly population the fastest growing segment of North American society, Alzheimer's threatens to be an even greater health concern in the future decades. For patients exhibiting mild cognitive impairment, research is being done on ways to slow the disease's progression. The two main thrusts of Alzheimer's research are biological, which seeks to determine organic, systemic contributing factors to the disease, and cognitive-behavioral, which examines whether the disease can be held at bay by engaging the brain in novel functions. Pharmaceutically, there are a few drugs approved for the treatment of Alzheimer's. These drugs just postpone the dementia-related declines, however, they don't offer any cure.

The most common symptom of Alzheimer's disease is a progressive dementia. The symptoms are mild at first, with the patient experiencing impaired memory function and inattention, and a difficulty performing everyday tasks. Because symptoms are initially mild, AD is frequently mistaken for normal decrements associated with aging. The ongoing brain damage that is occurring, however, leads to more severe symptoms. The AD patient will progress to a moderate dementia with (frequently) altered personality, difficulty with speaking or comprehension, and trouble moving. As the disease progresses, it becomes impossible for the Alzheimer's patient to be cared for at home, and the patient must enter a care facility. Eventually, the AD patient will become incontinent, unable to feed him or herself, and will eventually die. This progression from mild to moderate to severe, takes (on average) seven years, but may take as long as fifteen or twenty.

The diagnosis of Alzheimer's is a diagnosis of exclusion. Other causes of similar symptoms must be ruled out, such as vascular insult, malnutrition or adverse drug reactions. Autopsy is the only way to confirm diagnosis, by examining the brain damage that is characteristic of AD progression. One promising development in the area of Alzheimer's diagnosis is the use of the "Pittsburgh molecule." This process involves tagging a molecule that will bind with the amyloid plaques in the Alzheimer's patient's brain and allows it to be detected with a brain scan.

In the new test, patients are injected with a tiny amount of a harmless, radioactive molecule called Pittsburgh Compound B (PIB). PIB binds to protein aggregates called amyloid plaques that exist in the brains of those with Alzheimer's. The radioactive molecule can then be detected with a positron-emission tomography (PET) brain scan. (Pilcher, 2004).

The most characteristic aspects of an AD patient's brain are neurofibrillary tangles and amyloid plaques. The plaques that form in the brains of AD patients are composed of a protein called beta-amyloid, which are formed from a precursor, amyloid precursor protein (APP). These protein plaques are found predominantly in the brain's hippocampus, responsible for converting short-term memory into long-term. "In AD, plaques develop in the hippocampus, a structure deep in the brain that helps to encode memories, and in other areas of the cerebral cortex that are used in thinking and making decisions." (Rodgers, 2002, p22).

The other characteristic neuropathological feature of Alzheimer's is the formation of neurofibrillary tangles. These tangles involve another protein, tau. "In AD, tau is changed chemically. It begins to pair with other threads of tau and they become tangled up together. When this happens, the microtubles disintegrate." (Rodgers, 2002, p25). Although plaques and tangles may be present in a normal brain, to a limited extent, in AD, they overwhelm the neurons and their ability to function normally. "This hypothesized amyloid cascade underlies attempts to modify the onset and course of Alzheimer's disease through identification of antiamyloid agents, antioxidants [and] antiinflammatory drugs." (Cummings, 2004). It is normal for the human brain to change over time as a result of aging. However, Alzheimer's represents a decline that is a result of disease, not a normal progression.

No one is sure what causes Alzheimer's, although it is becoming apparent that AD is, at least in part, related to a genetic predisposition. Other, modifiable risk factors are being investigated. Some of the ongoing research into Alzheimer's involves a biological approach,...

"One [study] found that elevated levels of an amino acid called homocysteine, a risk factor for heart disease, are associated with an increased risk of developing AD." (Rodgers, 2002, p37). This finding may be significant, because homocysteine levels in the blood are, to an extent, available to external control. Vitamins, such as B6, B12 and folate have been shown to lower levels of homocysteine. There may also be a link between blood cholesterol levels and the development of Alzheimer's.
Perhaps related to the link between cardiovascular risk factors and AD is the finding in one study that moderate wine consumption correlates with lower rates of Alzheimer's. Wine has been found to have a beneficial impact on cardiovascular disease, when consumed in moderation, so this would appear to support the theory of a link between heart disease risk factors and AD.

Another avenue of promising biology-based AD research involves the effect free radicals may have on the development of Alzheimer's. Free radicals are a type of reactive oxygen species formed when a molecule has an unpaired electron in its orbital. This makes the species very reactive, and can be extremely harmful in the human body. In certain cases, free radical volatility is an asset, as it helps with the immune system response. Typically, however, excess free radicals result in oxidative damage to the surrounding tissue. There is some speculation that this damage could play a part in the progression of Alzheimer's.

This kind of damage is called oxidative damage. It may contribute to AD by upsetting the delicate machinery that controls the flow of substances in and out of the cell. The brain's unique characteristics, including its high rate of metabolism and its long-lived cells, may make it especially vulnerable to oxidative damage over the lifespan. (Rodgers, 2002).

Free radicals are an area of research being pursued in the causes and treatments of a variety of diseases. Much attention is being paid to the potential link between free radical damage and cancer. More research is needed into the role of oxidative damage in the development of Alzheimer's, although many are advocating the preventative approach of antioxidant therapy. Certain substances, such as selenium, Vitamin E and Vitamin C, have the ability to counter the oxidative effects of free radicals.

Many practitioners have added high-dose vitamin E supplements...to their standard treatment regimen for Alzheimer's disease... Several but not all epidemiologic studies provide evidence supporting the concept that vitamin E, as well as vitamin C, has a role in delaying the onset of Alzheimer's disease. (Cummings, 2004).

Recent research that supplementation with gingko biloba extract may also have beneficial effects on the cognitive functioning of Alzheimer patients. The mechanism of this potential improvement is not known, though there is speculation that it relates to the supplement's antioxidant properties. Although there are few conclusive clinical studies, antioxidant therapy is advocated by some as a means of potential Alzheimer's prevention.

The role of inflammation of the brain, and its link to Alzheimer's development and progression is also being investigated. Inflammation is a response of the immune system, usually to some kind of injury or foreign presence. Some research indicates that Alzheimer's may have some relationship to the immune system functioning. This is supported by findings that show lower rates of AD among people (primarily arthritis sufferers) who are taking NSAIDs (non-steroidal anti-inflammatory drugs). It is thought that by easing any inflammatory immune system response, the progression of AD may be slowed. This is still a speculative avenue of research and needs more scientifically rigorous support.

There is some question, also, about the efficacy of hormone therapy for the prevention of Alzheimer's. Initial research suggested that women taking estrogen supplements might have a slightly lower chance of being diagnosed with AD. Recently, however, studies point to an increased dementia risk for women on hormonal replacement. "Epidemiologic observations suggested that estrogen-replacement therapy might reduce the occurrence of Alzheimer's disease in postmenopausal women, but randomized, placebo-controlled trials of estrogen-replacement therapy in such women showed no benefit." (Cummings, 2004).

In addition to various biologically-based avenues of Alzheimer's Disease prevention and treatment, much of the research being done is also devoted to a consideration of cognitive-behavioral approaches to treat the dementia that is symptomatic of AD or provide a means of preventing the disease entirely.

One area of…