Alzheimer’s patients suffer from severe decline or loss of cognitive functions due to dysfunction and death of nerve cells, the major functioning cells in the brain. A key early event in Alzheimer's is increased production of a protein fragment, known as amyloid beta.

Normally, the amount of calcium inside cells is tightly controlled. Amyloid beta can disrupt this control and cause calcium overloading in cells. This, in turn, can cause nerve cell dysfunction and death. Scientists knowledge about what links amyloid beta to calcium and nerve cell death is still limited.

TRPM2 is a protein on the surface of cells that forms a channel. This channel regulates the flow of calcium in to and out of cells. There is evidence that activation of TRPM2 channels plays a role in Alzheimer’s by interacting with amyloid beta. This project aims to seek direct evidence to support this idea and thereby to better understand the exactly what causes Alzheimer’s disease.