Alzheimer’s disease (AD) is the most common form of dementia; estimates suggest that the incidence of AD will exceed 15 million by 2050 in North America alone. Due to the aging global population, AD is not only an immense socioeconomic burden, but also a major unmet global medical need. Regrettably,  no disease modifying therapeutics are currently available to prevent or delay AD. Currently approved AD treatments offer only temporary symptomatic relief.  There is an urgent need to identify new and alternative approaches to treat AD. 

Inflammation in the brain ("neuroinflammation") has been identified as a major component of  neurodegeneration.   We have collected compelling pre clinical data that demonstrates the target TRPM2 plays a critical role in driving neuroinflammation. Genetic removal of this target in cell and animal models of AD decreases neuroinflammation and improves disease progression.  Based on this, we have identified a novel class of small molecules that inhibit TRPM2 function. This project will enable us to develop these molecules into safe, selective and  brain penetrant therapeutics agents  that can be used reduce neuroinflammation and treat AD.