Amyloid beta, the principal component of senile plaques, is thought to be the pathogenesis of Alzheimer’s disease. The development of Alzheimer’s disease is associated with plaques and tangles in the brain. These plaques and tangles
Amyloid beta, the principal component of senile plaques, is thought to be the pathogenesis of Alzheimer’s disease. The development of Alzheimer’s disease is associated with plaques and tangles in the brain. These plaques and tangles are referred to as amyloids which are aggregates of proteins that become folded into a shape that allows many copies of that protein to stick together. The amyloid-cascade hypothesis states that the production and excessive accumulation of amyloid beta is the primary pathological event leading to Alzheimer’s disease. 1
The precursor to amyloid beta is Amyloid Precursor Protein (APP), which is endogenous in brain cells and is inert. The inert APP is converted by proteolytic enzymes by being cleaved by proteases in the secretase family, namely: 2
One of these three secretase enzymes is beta secretase (or BACE1). The initial stage of cleaving APP is done by beta secretase.
Thus a therapeutic strategy for Alzheimer’s disease is to inhibit over ex