Although the amyloid hypothesis has shifted its focus from plaque to soluble forms of Aβ, it largely remains defined by the central tenet that accumulation of amyloid, in a variety of forms, triggers a cascade that harms neurons and synapses.
The amyloid hypothesis postulates that amyloid-beta (Aβ), in a variety of forms, triggers a cascade harming synapses and ultimately neurons, producing the pathological presentations of Aβ plaques, tau tangles, synapse loss and neurodegeneration, leading to dementia.
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Instead, temperature, a major regulatory factor of the activity of this enzyme [4], [17], does not influence the oligomeric form triggered by a specific substrate.
When caspase 3 is cleaved, the activation form triggers apoptosis process [33].
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Aβ42, in contrast to Aβ40, is thought to be the pathogenic form triggering the pathological cascade in AD.
Thus a vicious cycle is formed, triggering an apoptosis process in the cells [ 48].
