Kinin B1 Receptor Mediated Neuroimmune Mechanisms of Alzheimer?s Disease Neuropathology

Alzheimer?s disease and related dementias has emerged as one of the major health challenges for aging populations, afflicting almost 50 million adults worldwide. The World Health Organization estimates that the prevalence of dementia worldwide will rise to 139 million people by 2050 as the population ages. Emerging evidence suggest that infection with SARS-CoV-2 is associated with acute and postacute neurological and neuropsychiatric symptoms, in long-term leading to long COVID, along with increased risk for the development of Alzheimer?s disease. Therefore, there is a critical need to understand how a single SARS-CoV-2 infection can cause long-term neurological consequences and predispose to Alzheimer?s disease pathology. In this proposal, we propose a novel hypothesis that SARS-CoV-2 induced neurological sequelae are mediated by B1R activation resulting in neuroinflammation and exacerbation of Alzheimer?s disease neuropathology leading to cognitive and neuropsychiatric deficits. This project addresses a highly novel role for B1R signaling and advances our fundamental understanding of neuro-immune interactions mediated by SARS-CoV-2 and provides insight for developing novel therapeutics to reduce the risk of developing Alzheimer?s disease.

Scholars @ ECU