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New Clues to Cause of Alzheimer’s

One of the outstanding features of the brains of persons with Alzheimer’s is the presence of amyloid beta plaques.  However, there is a small group of people whose brains contain these plaques, but who are free of the cognitive deficits displayed by those with Alzheimer’s.  And, up until now, the medical community has been at a loss to explain how this can happen.  But now, Dr. David Brody, associate professor of neurology, and his team of researchers at Washington University, in St. Louis, MO, have published the results of a study that may take a big step toward answering this question.

It appears now that the presence of these hard amyloid beta plaques in the brain is not sufficient, in and of itself, to produce Alzheimer’s symptoms.  One thing that this latest research does is point to the presence of smaller molecules of amyloid beta that are dissolved in the brain fluid, called amyloid beta “oligomers,” as being significant in the disease process.  It has been suspected, for some time, that these particles play a part in the presence of Alzheimer’s symptoms, but they have heretofore been too difficult to quantify.

Dr. Brody and his colleagues have developed a way to measure even small quantities of oligomers in brain tissue.  They looked at samples of brain tissue and fluid from 33 subjects (aged 74 to 107) at autopsy.  Ten of these subjects had no plaques and no dementia, fourteen had plaques but no dementia, and nine had plaques and dementia.

In comparison, all of the subjects who had beta amyloid plaques had relatively similar amounts of plaques.  However, those diagnosed with Alzheimer’s showed significantly more oligomers than those who did not show cognitive deficits.  It wasn’t the presence or absence of the oligomers that was significant, however.  Those with dementia symptoms were found to have a greater ratio of oligomers to plaques than those who did not show symptoms.

The researchers have speculated that, in those who had plaques but no symptoms, the plaques acted to capture the oligomers and prevent them from becoming problematic.  However, in those who were symptomatic the plaques have possibly exceeded their ability to filter out the oligomers, leaving them to float free in the brain fluid and interfere with the function of brain cells.

One word of caution here, from the researchers.  This is one study, done in the context of dissection during autopsy.  Results need to be verified through study of live subjects, possibly in a larger sample.  But it does suggest some possible avenues for further study.

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