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Home > News > Science > Microbiology/Genetics

August 10th, 2010, 15:01 GMT · By

Protein Fragments Found to Cause Cognitive Decline

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Amyloid levels in the brain are a clear indicator of cognitive decline
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A new study has revealed that high levels of beta-amyloid protein fragments in the plasma are related to a more rapid cognitive decline even in people who do not suffer dementia. Excess beta-amyloid concentrations are generally the hallmark of Alzheimer's disease.

However, the research team behind the new work argues that proteins can accumulate in the human brain even without the affected individual suffering from Alzheimer's, or other forms of dementia. A full report on the work will appear in the December print issue of journal Archives of Neurology.

“Examination of specific cognitive domains in the current study revealed that global cognitive change in healthy elderly individuals was driven primarily by memory, rather than language or visuo-spatial abilities,” the investigators write in the journal entry.

“This seemingly selective association with memory has several interpretations. First, it may suggest that healthy elderly people with a high-risk beta-amyloid profile are in the early stages of Alzheimer's disease but have not yet demonstrated sufficient change in non-memory domains to meet criteria for dementia,” they say.

The work was authored by Columbia University Medical Center expert Stephanie A. Cosentino, PhD. She also holds an appointment at the Taub Institute for Research in Alzheimer's Disease and the Aging Brain, in New York. The expert and her group analyzed some 880 test subjects.

It became immediately apparent in the work that keeping an eye on amyloid levels could easily inform healthcare experts about the cognitive decline each of the participants was exhibiting. The correlation was found to exist independent of the development of Alzheimer's or other forms of dementia, ScienceDaily reports.

“Stated differently, the observable change in both plasma beta-amyloid and memory in this group could be a fundamentally different process than that involved in Alzheimer's disease or might fall short of a critical threshold beyond which the full pathological presentation and clinical dementia syndrome of Alzheimer's disease would unfold,” the experts write.

“It is thus important for future work to determine more definitively the specificity of beta-amyloid profiles for predicting dementia vs. their significance for cognitive aging more generally,” they conclude. The research was funded with grant money awarded by the National Institutes of Health (NIH).

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