Understanding the relationship between our immune response and Alzheimer’s disease

Alzheimer’s disease involves the build-up of a protein called amyloid in the brain which goes on to trigger other harmful processes and ultimately leads to damage to brain cells. Research has shown that amyloid interacts with other cells involved with our immune response and can cause it to switch from being protective to destructive.

Previous work by Prof Clare Bryant and her team showed that amyloid activates a protein called TLR4 to change its function. Normally, TLR4 helps to protect the brain from infections, but in the presence of amyloid it sends messages to the brain’s immune cells, stops their normal protective function, and instead causes sustained inflammation. This can cause damage to cells over a long period of time.

Prof Bryant has received a Major Project Grant which will allow her team to investigate how amyloid interacts with TLR4 protein to cause inflammation in the brain. Their aim is to understand how amyloid affects TLR4 to make it stop its normal function and what signals trigger the ongoing inflammation.

There have been many clinical trials that have tested new treatments to try and stop the progression of Alzheimer’s, and research is bringing us closer to breakthroughs. By understanding how the interaction between amyloid and TLR4 works, the team want to identify potential new drug targets that could control inflammation and prevent the damage to the brain.