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Cortex Area Thinner in Youth with Alzheimers-Related Gene

BETHESDA, Md., April 23, 2007--A part of the brain first affected by Alzheimers disease (http://www.nia.nih.gov/Alzheimers/) is thinner in youth with a risk gene for the disorder, a brain imaging study by researchers at the National Institute of Mental Health (NIMH), one of the National Institutes of Health (NIH), has found. A thinner entorhinal cortex, a structure in the lower middle part of the brains outer mantle, may render these youth more susceptible to degenerative changes and mental decline later in life, propose Drs. Philip Shaw, Judith Rapoport, Jay Giedd, and NIMH and McGill University colleagues. They report on how variation in the gene for apoliproprotein (ApoE), which plays a critical role in repair of brain cells, affects development of this learning and memory hub in the June, 2007 Lancet Neurology.

People with the Alzheimers-related variant of the ApoE gene might not be able to sustain much aging-related tissue loss in the entorhinal cortex before they cross a critical threshold, explained Shaw. But the early thinning appears to be a harmless genetic variation rather than a disease-related change, as it did not affect youths intellectual ability. Only long-term brain imaging studies of healthy aging adults will confirm whether this anatomical signature detectible in childhood predisposes for Alzheimers.

It was already known that adults destined to develop Alzheimers disease tend to have a smaller and less active entorhinal cortex (http://www.nia.nih.gov/Alzheimers/ResearchInformation/NewsReleases/Archives/PR2000/PR20000329MRI.htm). This structure is the first to shrink in volume and to develop the neurofibrillary tangles (




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