Much research continues to be done into what causes Alzheimer's Disease, in the hope of developing treatments to slow or interrupt the disease process. Not enough is known at this stage to prevent or to cure the disease.

CHANGES IN THE BRAIN

We know much about what happens to the brain - but is this cause or effect?
The symptoms of Alzheimer's Disease are related directly to changes in the brain. Most dementias follow the same pathway. Brain cells (neurones) degenerate, lose their ability to communicate and die. Because your brain can't replace nerve cells, some brain function is lost. Autopsies and microscopic examination of the brains of Alzheimer's patients reveal the presence of senile plaques and what are termed neurofibrillary tangles throughout brain cells. The plaques are mainly composed of a protein called beta.amyloid Beta amyloid protein is secreted by cells throughout the body, but is produced in particularly large amounts in the brain. In those with Alzheimer's Disease, the plaques develop in the spaces (synapses) between the brain cells early in the disease process, before any surrounding neurone damage is evident and years before symptoms develop.

Some Alzheimer's patients lack fibrous beta amyloid, so research is also investigating the role of related proteins (called beta amyloid diffusible ligands or ADDLs) in memory loss. The tangles result from alterations in another protein called tau, which is an important part of the internal support structure of nerve cells. It is known that, in the brains of Alzheimer's sufferers, threads of this protein become twisted and that this seriously damages the nerve cells, ultimately causing them to die. But are these abnormalities the cause of the disease or a result of it? Scientists suspect that these fibres kill brain cells and erode the brain's ability to store memories. Scientists still aren't certain exactly how plaques and tangles are involved in Alzheimer's or what causes them to occur. Pharmaceutical companies are working on drugs they hope will prevent beta amyloid accumulation in the brain.

Alzheimer's patients also have a noticeable drop in levels of neurotransmitters - the chemicals that send messages across the gaps between nerve cells (synapses). This means that nerve pathways cannot function efficiently. In 1976, researchers discovered that levels of the neurotransmitter, acetylcholine dropped up to 90 percent in people with Alzheimer's. But scientists now think the decrease in acetylcholine and other neurotransmitters may happen late in the disease, and that the neurotransmitter decline may actually be a result of the disease process rather than a cause.

LOOKING FOR PREDICTORS

The search is on an indicator which could allow early diagnosis.
Researchers hope to find a measurable change in brain chemistry which could predate memory loss. This could then be used as an indicator early in the disease, especially in those whose family history make them high risk candidates. Currently, doctors diagnose Alzheimer's after a person experiences memory or other cognitive disorders. Researchers have found that people who are genetically at high risk for the development of Alzheimer's have measurable chemical abnormalities in their brains that pre-date evidence of memory disorder. One protein being studied is a specific type of cholesterol-carrying protein called apolipoprotein E 4 (APOE 4) which is believed to be a strong predictor for Alzheimer's in people with mild memory loss.

The APOE gene has also been the focus of major genetic research. A form of this gene has been linked to increased blood levels of the amyloid protein which forms Alzheimer's plaques and tangles in the brain. What causes the protein to accumulate in people with the more common, non-inherited form of Alzheimer's is unknown. Most experts now believe that people who have this form of the APOE gene are at increased risk for early onset Alzheimer's Disease. But doctors warn that testing for the gene is not yet reliable for diagnosing or predicting the disease.

PREVENTION

There is no known way of preventing Alzheimer's Disease.
Lifestyle factors like diet and exercise levels may play a role, just as they do in general maintenance of health. With Alzheimer's Disease, a disease of the brain, mental fitness may prove to be important in delaying onset of dementia in some. One research study focused on a large order of nuns who have significantly lower rates of Alzheimer's, even though their average age is 85 and many are in their 90s. Many of the nuns have advanced academic degrees and led an intellectually challenging life into old age. This has led researchers to believe that lifelong mental exercise and learning and the associated brain activity may delay the onset of dementia.

TREATMENT

Research is being undertaken into a variety of treatments.
Treatment of Alzheimer's Disease is still in its early stages, with no definitive preventions or treatments being in place. Most of the prescribed drugs are still in some stage of testing. All, including the few currently available, are designed to treat some of the manifestations of the disease. None offers a cure of the underlying illness. There are, however, a number of drug therapies being investigated which may prove effective in delaying the onset of the mental deterioration the disease causes.

A number of treatments are currently under investigation.
A number of alternative therapies are also promoted by some.

Doctors need a complete knowledge of all medications being taken.
Doctors may prescribe drugs to treat associated symptoms of the disease such as depression or agitation. Doctors should be kept aware of all drugs being taken, including over the counter medications, and patients should be monitored closely for side effects. Many older adults may have reactions to medications, including over-the-counter drugs, that they're taking. Sometimes symptoms can be improved by adjusting the dose or changing when or in what combinations drugs are taken. Those who seek information about prescription drugs and their possible side effects can visit the following

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