A team of neuroscientists has identified a modification to a protein in laboratory mice linked to conditions associated with Alzheimer's Disease. Their findings, which appear in the journal Nature Neuroscience, also point to a potential therapeutic intervention for alleviating memory-related disorders.
The research centered on eukaryotic initiation factor 2 alpha (eIF2alpha) and two enzymes that modify it with a phosphate group; this type of modification is termed phosphorylation. The phosphorylation of eIF2alpha, which decreases protein synthesis, was previously found at elevated levels in both humans diagnosed with Alzheimer's and in Alzheimer's Disease (AD) model mice.
"These results implicate the improper regulation of this protein in Alzheimer's-like afflictions and offer new guidance in developing remedies to address the disease," said Eric Klann, a professor in New York University's Center for Neural Science and the study's senior author.
The study's co-authors also included: Douglas Cavener, a professor of biology at Pennsylvania State University; Clarisse Bourbon, Evelina Gatti, and Philippe Pierre of Universit de la Mditerrane in Marseille, France; and NYU researchers Tao Ma, Mimi A. Trinh, and Alyse J. Wexler.
It has been known for decades that triggering new protein synthesis is vital to the formation of long-term memories as well as for long-lasting synaptic plasticity -- the ability of the neurons to change the collective strength of their connections with other neurons. Learning and memory are widely believed to result from changes in synaptic strength.
In recent years, researchers have found that both humans with Alzheimer's Disease and AD model mice have relatively high levels of eIF2alpha phosphorylation. But the relationship between this characteristic and AD-related afflictions was unknown.
Klann and his colleagues hypothesized that abnormally high levels of eIF2alpha phosphoryl
|Contact: James Devitt|
New York University