Researchers do not know the exact cause of Alzheimer’s disease, but it likely is due to a variety of genetic and environmental factors. The most studied of the environmental factors are aluminum, zinc, food-borne poisons, and viruses.
Aluminum
One of the most publicized and controversial theories concerns aluminum, which became a suspect in Alzheimer’s disease when researchers found traces of this metal in the brains of patients with Alzheimer’s disease. Many studies since then have either not been able to confirm this finding or have had questionable results.
Aluminum does turn up in higher amounts than normal in some autopsy studies of Alzheimer’s patients, but not in all. Further doubt about the importance of aluminum stems from the possibility that the aluminum found in some studies did not all come from the brain tissues being studied. Instead, some could have come from the special substances used in the laboratory to study brain tissue.
Aluminum is a common element in the Earth’s crust and is found in small amounts in numerous household products and in many foods. As a result, there have been fears that aluminum in the diet or absorbed in other ways could be a factor in Alzheimer’s. One study found that people who used antiperspirants and antacids containing aluminum had a higher risk of developing Alzheimer’s. Others have also reported an association between aluminum exposure and Alzheimer’s disease.
On the other hand, various studies have found that groups of people exposed to high levels of aluminum do not have an increased risk. Moreover, aluminum in cooking utensils does not get into food and the aluminum that does occur naturally in some foods, such as potatoes, is not absorbed well by the body. On the whole, scientists can say only that it is still uncertain and rather unlikely that exposure to aluminum plays a role in Alzheimer’s disease.
Zinc
Zinc has been implicated in Alzheimer’s disease in two ways. Some reports suggest that too little zinc is a problem, others that too much zinc is at fault. Too little zinc was suggested by autopsies that found low levels of zinc in the brains of Alzheimer’s disease patients, especially in the hippocampus.
On the other hand, a recent study suggests that too much zinc might be the problem. In this laboratory experiment, zinc caused soluble beta amyloid from cerebrospinal fluid to form clumps similar to the plaques of Alzheimer’s disease. Current experiments with zinc are pursuing this lead in laboratory tests that more closely mimic conditions in the brain.
Food-borne poisons
Toxins in foods have come under suspicion in a few cases of dementia. Two amino acids found in seeds of certain legumes in Africa, India, and Guam might cause neurological damage. Both enhance the action of the neurotransmitter glutamate, also implicated in Alzheimer’s disease.
In Canada, an outbreak of a neurological disorder similar to Alzheimer’s occurred among people who had eaten mussels contaminated with demoic acid. This chemical, like the legume amino acids, is a glutamate stimulator. While these toxins might not be a common cause of dementia, they could eventually shed some light on the mechanisms that lead to neuron degeneration.
Viruses
In some neurological diseases, a virus is the culprit, lurking in the body for decades before a combination of circumstances stirs it to action. For years, researchers have sought a virus or other infectious agent in Alzheimer’s disease.
This line of research has yielded little in the way of hard evidence so far, although one study in the late 1980s did provide some data that have kept the possibility alive. In general, however, the likelihood of a viral etiology is considered remote.
Zinc has been active in Alzheimer’s ache in two ways. Some letters advance that too little zinc is a problem, others that too abundant zinc is at fault. Too little zinc was appropriate by autopsies that begin low levels of zinc in the accuracy of Alzheimer’s ache patients, abnormally in the hippocampus.
On the added hand, a contempo abstraction suggests that too abundant zinc ability be the problem. In this class experiment, zinc acquired acrid beta amyloid from cerebrospinal aqueous to anatomy clumps agnate to the plaques of Alzheimer’s disease. Current abstracts with zinc are advancing this advance in class tests that added carefully actor altitude in the brain.
Food-borne poisons
Toxins in foods accept appear beneath suspicion in a few cases of dementia. Two amino acids begin in seeds of assertive legumes in Africa, India, and Guam ability could could could could cause acoustic damage. Both enhance the activity of the neurotransmitter glutamate, aswell active in Alzheimer’s disease.
In Canada, an beginning of a acoustic ataxia agnate to Alzheimer’s occurred a part of humans who had eaten mussels attenuated with demoic acid. This chemical, like the legume amino acids, is a glutamate stimulator. While these toxins ability not be a accepted could could could could cause of dementia, they could eventually afford some ablaze on the mechanisms that advance to neuron degeneration.
Viruses
In some acoustic diseases, a virus is the culprit, ambuscade in the physique for decades afore a aggregate of affairs stirs it to action. For years, advisers accept approved a virus or added communicable abettor in Alzheimer’s disease.
This band of analysis has yielded little in the way of harder affirmation so far, although one abstraction in the backward 1980s did accommodate some abstracts that accept kept the achievability alive. In general, however, the likelihood of a viral analysis is advised remote.
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