Printer Friendly

Aging brains similar to diseased ones.

Alzheimer's disease and frontotemporal lobar degeneration (FTLD) are two of the most prevalent forms of neurodegenerative disorders. In a study published in Genome Research, scientists have analyzed changes in gene expression in aging and diseased brains, finding new clues to the biology of normal aging and neurodegenerative diseases.

Recent studies have identified changes in how genes are read, or expressed, in the brain either during aging or with neurodegenerative disease. However, no previous study directly had compared gene expression changes in healthy aging with those in diseased individuals.

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 those from diseased patients, 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," relates senior author Jernej Ule of MRC Laboratory of Molecular Biology, Cambridge, U.K.

Aging-related changes were apparent in the diseased individuals as young as 50 years--"roughly 25 years before we would expect to see similar changes in healthy individuals," indicates James Tollervey of MRC, the first author of the study.

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 an RNA molecule are arranged differently to change the message, which potentially can be harmful if misregulated.

In normal aging, changes in alternative splicing largely affect genes associated with cellular metabolism, while disease-specific alterations are 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 likely is 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 normal aging and neurodegenerative disease. "These findings," declares Ule, "indicate that studies of healthy aging could help unravel the processes that lead to neurodegeneration."

"Conversely, our findings also suggest that studies of neurodegenerative diseases might help us understand how to delay the changes that take place in healthy individuals at an advanced age," notes study coauthor Boris Rogelj of the MRC Centre for Neurodegeneration Research at King's College, London.

COPYRIGHT 2011 Society for the Advancement of Education
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2011 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Neurodegenerative Disorders
Publication:USA Today (Magazine)
Geographic Code:1USA
Date:Oct 1, 2011
Words:423
Previous Article:Lack of symptoms could prove deadly.
Next Article:Genetic variation linked to sudden cardiac arrest.
Topics:

Terms of use | Copyright © 2017 Farlex, Inc. | Feedback | For webmasters