Alzheimer’s disease is one of the most common age degenerative neurological diseases. It is characterized by the presence of amyloid deposition, neurofibrillary tangles, progressive loss of synapses and severe cognitive dysfunction. The composition of amyloid peptides are known to be the early events that could potentially lead to Alzheimer’s Disease pathologies, and the impairment of synaptic function.
To understand why this treatment is able to combat Alzheimer’s disease the way that it does it is important to understand why BACE1 inhibition is as effective as it is, along with the downsides of BACE1 inhibition. The production of Aβ (amyloid beta) requires β-secretase, also called β-site amyloid precursor protein (APP)–cleaving enzyme 1 (BACE1), which cleaves APP to release a soluble N-terminal fragment and a membrane- anchored C-terminal fragment.
This will further cleave the C-terminal fragment by γ-secretase removing Amyloid beta. Such Genetic mutations like the K670M671 to N670L671 mutation or the A673 to T673 mutation can either increase or decrease Aβ generation, resulting in early- onset AD or protection against developing AD. Mice that were deficient in BACE1 had shown few traces of amylase beta. This means that it could reduce amylase plaques which could impair synaptic functions. It goes to show that BACE1 is an important target to take into account when treating Alzheimer’s disease.
We could potentially use this information to not only treat Alzheimer’s disease, but curing the disease within itself at the early stages of its development. This stands to be a great stride in Alzheimer’s treatment, and will hopefully be fully developed in our lifetime.
