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Last updated on April 20, 2014 at 19:30 EDT

New Link Between Alzheimer’s and Healthy Aging

August 18, 2011

(Ivanhoe Newswire) — Alzheimer’s disease and frontotemporal lobar degeneration (FTLD) are two of the most prevalent forms of neurodegenerative disorders. Researchers have analyzed changes in gene expression in the aging and diseased brain, finding new clues to the biology of normal aging and neurodegenerative diseases.

In this report, an international team of researchers analyzed and compared changes in gene expression associated with aging and disease in a region of the brain known to be affected in both Alzheimer’s and FTLD. Comparing samples from healthy individuals ranging from 16 to 102 years old with samples from diseased individuals, the investigation uncovered striking similarity in the changes in gene expression patterns associated with aging and the neurodegenerative diseases.

“Surprisingly, these [diseased] samples contained the same aging-related changes as healthy individuals over the age of 80,” Dr. Jernej Ule of the MRC Laboratory of Molecular Biology, senior author of the study, was quoted as saying.

“Aging-related changes were apparent in the diseased individuals as young as 50 years,” Dr. James Tollervey of the MRC Laboratory of Molecular Biology, the first author of the study, was quoted as saying, “roughly 25 years before we would expect to see similar changes in healthy individuals.”

While the similarities were striking, the group also observed notable differences between gene expression in the normal aging brain and expression in Alzheimer’s and FTLD, particularly in the patterns of alternative splicing, a process by which parts of a RNA molecule are arranged differently to change the message, which can be potentially harmful if misregulated.

In normal aging, changes in alternative splicing largely affected genes associated with cellular metabolism, while disease-specific changes were associated with genes involved in neuron-specific function. The group found that there were changes in the expression of several genes coding for RNA binding proteins, which is likely responsible for at least part of the observed alterations in splicing.

The authors expect that this work will have broad impact for further insight into both normal aging and neurodegenerative disease. “These findings indicate that studies of healthy aging could help unravel the processes that lead to neurodegeneration,” said Dr. Ule.

SOURCE: Genome Research, published online August 18, 2011