Fighting Alzheimer’s with ‘decoy receptors’

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by memory loss that currently has no cure.
Part of the reason we don’t have a cure is because we don’t know exactly how the disease works. From what we can tell, there is a build up of a protein called beta-amyloid, and that as the amount of this protein builds up, nerve cells begin to die.
Researchers at the University of Florida have been investigating the immune response to Alzheimer’s and how it may help us treat the condition in the future.
Their research has focused around a particular immune cell called microglia, whose responsibility is to clear toxins and debris (such as beta-amyloid) from the brain. In Alzheimer’s disease the microglia don’t function as they should, which is believed to be at least partially due to the plaque buildups causing inflammatory damage.
In order to protect the microglia from this damage, the research team looked at the effects of a family of proteins called “toll-like receptors” or TLRs. These immune cell surface receptors react to damage cells or floating debris, leading to an immune response.
They postulated that if they could remove some of the TLRs from the surface of the microglia, the now free floating TLR’s would serve as ‘decoys’ and be able to bind the amyloid proteins before they had the chance to aggregate.
They demonstrated this by separating the TLR5 receptor from microglia in a mouse model, which prevented, and even possibly reversed plaque buildup.
While this is only the beginning, the ability to use TLR5 decoy receptors to deplete or prevent build-up of these plaques is promising research, and will surely spark deeper investigation.
For more information, please visit MedicalNewsToday.
Questions: Are you excited about this new direction in the Alzheimer’s disease research?
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