Noncoding Translation Feedback Loop in Alzheimer’s Disease

Alzheimer’s disease (AD) primarily arises from the accumulation of plaques in the brain. Despite decades of dedicated academic and pharmaceutical research, efforts to clear these plaques have seen limited success, yielding only modest benefits. This limited efficacy may stem from the presence of self-sustaining pathological processes, which initially are triggered by the plaques but subsequently operate independently of them. Identifying and understanding these self-reinforcing feedback loops is critical for advancing novel AD therapies. In this study, our objective is to investigate one such feedback loop that exacerbates errors in gene expression. We will employ genomic techniques to scrutinize human AD brain samples, followed by validation through experiments conducted on mouse models of AD.