Study published in the Journal of Neuroscience finds that APP needs to work with Reelin.

A team of investigators discovered that amyloid precursor protein (APP) interacts with another protein known as Reelin to promote formation and maintenance of dendrites. Results are reported in the June 10 issue of the Journal of Neuroscience.

Reelin has been thought to be involved in stimulating growth of neuronal dendrites. It also has been implicated in some brain disorders, but up until now, little was known about how the protein interacts with APP, the scientists point out.

Trying to understand how APP works in the brain and the interplay with Reelin, the researchers studied neurons in culture. They found that adding Reelin increased the number of neurite connections that these cells sent out from the cell body to communicate with each other. However, these branches did not grow if APP was not available.

In mice experiments, they found that animals born without APP had increased levels of Reelin, and mice that overproduced APP had less Reelin. “This suggests that two molecules are necessary for a single function, and if you get rid of one of them, the other increases in order to drive that function,” says the study’s senior author, G. William Rebeck, Ph.D., associate professor in the department of neuroscience at Georgetown University Medical Center.

While Dr. Rebeck’s previous research found that APP is important for the stability of dendrites, this study shows that it is also key to their formation and maintenance. Findings may not be immediately applicable to the treatment of Alzheimer’s but help elucidate the workings of components related to the disease, he adds.

Related News

Two Proteins Working in Tandem Leads to Amyloid Beta Buildup in Alzheimer’s (Dec. 22, 2008)
miRNA Implicated in Inflammation Integral to Alzheimer’s Disease (Nov. 14, 2008)
Fatty-Acid Regulator Associated with Cognitive Function in Alzheimer’s Disease (Oct. 20, 2008)
Variations in Tau Gene Linked to Earlier Onset of Alzheimer’s Symptoms (June 10, 2008)
Inhibiting TGF-beta Improves Immune Response to Alzheimer’s Plaques (May 30, 2008)

Previous articleICON Tasked with Clinical Trial Site Setup and Monitoring for Lilly in Europe
Next articleEU Countries Commit to Implement National Plans for Rare Diseases