American and Chinese scientists reported on Wednesday in the journal Neuron how a receptor on the immune cell in the brain helps prevent or reduce severity of Alzheimer's disease, a neurodegenerative disorders affecting 47 million people worldwide.
The study, led by Xu Huaxi, a neuroscientist from Sanford Burnham Prebys Medical Discovery Institute, has shown that a receptor called TREM2 can interacts with toxic amyloid beta proteins to restore neurological function.
Xu said, TREM2 can bind specifically to oligomers of amyloid beta, the main component of the plaques found in the brains of Alzheimer's patients.
An increasing TREM2 level renders the immune cell called microglia more responsive and reduces Alzheimer's disease symptoms. Microglia is a brain cell known to be able to eat up amyloid beta.
Without TREM2, however, microglia were much less successful at binding to, and clearing out, amyloid beta. Also, removing TREM2 downregulates microglial potassium ion channels, thus impairing the electrical currents associated with the activation of these immune cells.
"This new research reveals specific details about how TREM2 works, and supports future therapeutic strategies to strengthen the link between amyloid beta and TREM2," said Xu.
Researchers found that the added TREM2 signaling stopped disease progression and even restored cognitive function.
"Going after microglia, rather than amyloid beta generation, may be a new research avenue for Alzheimer's disease," said Xu.
Researchers from Fujian Medical University, Xiamen University, University of Texas and University of California Los Angles participated in the study.
