A recent study conducted at the Nathan S. Kline Institute for Psychiatric Research (NKI) and the NYU Langone Medical Center implicates a new culprit in Alzheimer's disease (AD) development. The research reveals that C-terminal fragment beta (beta-CTF) -- 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. Results from the study were published online on July 21, 2015 in the journal, Molecular Psychiatry, and the article has been selected for an issue cover. The article is titled “De Novo Deleterious Genetic Variations Target a Biological Network Centered on Aβ Peptide in Early-Onset Alzheimer Disease.” The recent study findings involving beta-CTF have significant implications for treatment strategies and furthering the course of Alzheimer's drug development. Presently, the most common strategy for treating AD is targeting the amyloid beta peptide, which has had modest success in clinical trials. Findings from this new research suggest that drugs that may reduce beta-CTF levels as well as beta-amyloid, such as the class of BACE1 inhibitors currently under development, may help slow or stop the progression of AD. Beta-CTF is formed during endocytosis, the process by which cells absorb nutrients and sample various materials from the outside environment. It has been known for some time that abnormalities of endocytosis develop very early in AD, well before clinical symptoms, and that variant forms of genes controlling endocytosis are frequently implicated as risk factors promoting Alzheimer's.
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