Jan. 11 (UPI) -- Researchers in Beligium reported Friday they have located a key receptor in the brain that plays a role in Alzheimer's disease, which they say may lead to better treatments for it.
The amyloid precursor protein regulates neuronal signal transmission by connecting to a specific receptor, with the researchers suggesting that a method for regulating it could improve Alzheimer's treatment, according to findings published Friday in the journal Science.
"We knew that the amyloid precursor protein exerts its role through the part of the protein that is released outside of the cell. To understand its function, we needed to look for binding partners located on the cell surface," Heather Rice, a researcher at the VIB-KU Leuven Center for Brain & Disease Research and study author, said in a news release.
The researchers think these new findings will shed light on old research about the amyloid precursor protein and Alzheimer's disease.
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More than 30 years ago, scientists first linked the amyloid precursor protein to a gene found on chromosome 21. Subsequent research has helped explain what the rest of the amyloid precursor protein actually does.
"We found that the secreted part of the amyloid precursor protein interacts with a receptor called GABABR1a, and that this in turn suppressed neuronal communication at the synapse," Rice said.
An estimated 5.7 million Americans have Alzheimer's disease, according to the Alzheimer's Association.
"Although mutations in the amyloid precursor protein in familial cases of Alzheimer's disease all affect the production of amyloid-β, we don't really know whether other aspects of the protein's function contribute to Alzheimer's as well," said Bart De Strooper, the VIB-KU Leuven Center for Brain & Disease Research.
"The newly identified role of the amyloid precursor protein may underlie the neuronal network abnormalities we see in mouse models of Alzheimer's disease and preceding clinical onset in human patients. It is exciting to consider that a therapy targeting this receptor might attenuate these abnormalities in people with Alzheimer's."
