Subject:  Alzheimer's Disease, contributing factor....
Date:     Wed, 21 Oct 1998 144708 -0500 (CDT)
From:     "Roy L. Beavers" <rbeavers@llion.org>
To:       emfguru <rbeavers@llion.org>
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.......Some epidemiological studies have found an association
between EMF and Alzheimer's.....The speculation has centered on
the possible impact of EMF on brain neurons......When (and IF!!)
EMF research is resumed, this aspect is certainly an area that
should be pursued.....guru.....

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11:50 AM ET 10/21/98

Brain plaque linked to cell death in Alzheimer's

        
          (Release at 1800 GMT, Oct 21)
            By Patricia Reaney
            LONDON, Oct 21 (Reuters) - Swiss scientists have come a step
closer to understanding how Alzheimer's disease, the commonest
form of dementia, affects the brain.
            By injecting mice with a mutant human gene involved in the
illness they have shown for the first time that the buildup of
plaque in the brain, a characteristic of Alzheimer's disease, is
related to brain cell death, or neuron loss.
            ``Amyloid plaque formation alone, just this one aspect of
Alzheimer's disease, leads to neuron loss which is one of the
major pathologies of the disease,'' Matthias Jucker, of the
University of Basel, said in a telephone interview on Wednesday.
            Alzheimer's disease causes a slow deterioration of the brain
and a corresponding loss of memory and mental functions.
Scientists have already identified genes that play a part in the
disorder but they are only beginning to understand how.
            Jucker and his colleagues believe their transgenic mice
could speed up the process and provide an important mechanism
for developing and testing new drugs aimed at reducing or
stopping the formation of plague and cell death.
            In a letter to the science journal Nature, Jucker and his
team described how they injected the mice with the mutant APP
gene. It is one of the genes involved in the development of
early-onset Alzheimer's disease that runs in families. Although
familial Alzheimer's accounts for only 10 percent of all cases
scientists believe the progression of the disorder is similar in
most sufferers.
            Jucker and his team found that neuron loss in the transgenic
mice was greater than in healthy mice and was much higher in
mice with more brain plaque.
            ``We have shown that the formation of amyloid plaques can
lead to region-specific loss of neurons in a transgenic mouse,''
Jucker added.
            In addition to its importance in the development and testing
of new drugs for Alzheimer's disease, the scientists said the
finding will allow them to study how plaque is related to brain
cell death.
            ``Now we can study the mechanism of how it happens. Until
now we did not have an animal model with amyloid plaques and
neuron loss. Now we have it.''
            In a separate study, researchers from the University of
Oxford found that boosting levels of vitamin B12 and folic acid
may help to prevent the onset of Alzheimer's disease.
            The Optima project on ageing and the brain examined annual
blood samples of hundreds of people. They found that people with
low levels of vitamin B12 and folic acid in their blood were
more likely to develop the disorder than those with higher
levels.
            There also seemed to be a link between vitamin B12 and folic
acid and homocysteine, an amino acid. People with lower levels
of the vitamin and folic acid had higher levels of the amino
acid, which is associated with a greater risk of getting the
disease.
            David Smith, the head of the Optima project, said it was not
clear yet if the differences in B12, folic acid and homocysteine
were a cause of Alzheimer's disease or a consequence. But the
levels in the patients remained constant despite the progress of
the illness, suggesting they were a cause of the disease.
            Alzheimer's disease affects one percent of 60-64 year-olds,
five percent of people over the age of 65 and 20 percent of
those over 80. There is no cure but drugs can slow the
progression of the illness.
 ^REUTERS@




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Reprinted with permission of Roy Beavers, http://www.feb.se/EMF-L/EMF-L.html