Researchers Identify New Potential Biotherapy for Alzheimer's Disease

A study published in the Journal of Experimental Medicine reveals that soluble versions of a protein or toll-like receptors (TLR) called TLR5 can reduce the accrual of amyloid plaques in the brains of Alzheimer's disease model mice and prevent the peptide forming these plaques from killing neurons, reports EurekAlert . The researchers theorized that untethering some of these TLRs from the surface of microglia could reduce amyloid plaque formation, perhaps functioning as "decoy receptors" that bind to ß-amyloid and constrain its aggregation without initiating cellular signaling pathways that could cause inflammation. The team demonstrated that soluble TLR5 could bind to ß-amyloid aggregates and augment their uptake into microglia, while also reducing the ability of ß-amyloid to destroy neurons cultured in the laboratory. "This mouse model is well recognized as a primary model for Alzheimer-type amyloid plaque deposition, but it does not recapitulate the entire Alzheimer's neurodegenerative cascade," says the University of Florida's Paramita Chakrabarty. "Therefore, the potential of soluble TLR5 in dampening immune activation and related neurotoxic pathways needs to be further explored in multiple models of Alzheimer's disease."