Researchers from the University of California, San Diego School of Medicine have identified a protein which, when over-expressed, leads to the formation of senile plaques that cause Alzheimer's disease.
It can be a potential new therapeutic target to block the accumulation of amyloid plaque in the brain.
"The role of the multi-domain protein, RANBP9, suggests a possible new therapeutic target for Alzheimer's disease," said Dr David E. Kang, assistant professor of neurosciences at UC San Diego and director of this study.
The researchers identified the RANBP9 protein by studying low density lipoprotein receptor-related protein (LRP), a protein that rapidly shuttles Aß out of the brain and across the blood-brain barrier to the body, where it breaks down into harmless waste products.
"RANBP9 is one of the proteins we identified that interacted with this LRP segment, but one that had never before been associated with disease-related neuronal changes," said Kang.
"We discovered that this protein interacts with three components involved in Aß generation - LRP, APP and BACE1 - and appears to 'scaffold' them into a structure," he added.
When the scientists knocked out RANBP9 in the cell, 60pct less Aß was produced.
"Inhibiting the RANBP9 protein may offer an alternative approach to therapy, by preventing contact between APP and the enzyme that makes the cut essential to produce amyloid plaques."
The researchers will be conducting further studies to verify these findings in animal models.
The study will be published in the Journal of Biological Chemistry.