LOS ANGELES: A recent study conducted at Nathan S. Kline Institute for Psychiatric Research (NKI) and NYU Langone Medical Center implicates a new culprit in Alzheimer’s disease development. The research reveals that ßCTF – the precursor of the amyloid beta (Aß) peptide – acts at the earliest stage of Alzheimer’s to initiate a range of abnormalities leading to the loss of groups of neurons critical for memory formation.
The recent study findings involving ßCTF have significant implications for treatment strategies and furthering the course of Alzheimer’s drug development. Presently, the most common strategy for treating Alzheimer’s disease is targeting the amyloid ß peptide, which has had modest success in clinical trials. Findings from this research suggest that drugs that may reduce βCTF levels as well as beta-amyloid, such as the class of BACE1 inhibitors currently under development, may help slow or stop the progression of Alzheimer’s disease.