These include T - cell
depletion by apoptosis; anergy (ie, the process by which T cells that are presented with a peptide in the absence of costimulatory signals become refractory to further stimulation with the antigen and are therefore inactivated); and the development of regulatory T cells, which can actively suppress antigen - specific responses following re-challenge with the antigen.
Enhanced amyloidogenic processing of APP
by the ß - site APP cleaving enzyme (BACE) and the γ - secretase complex and reduced clearance lead to increased intracellular levels of soluble oligomeric Aß, resulting in cellular dysfunction comprising e.g., synaptic failure, mitochondrial dysfunction, enhanced oxidative stress, neurotransmitter and neurotrophin
depletion, inflammation, and
apoptosis which is reflected in patients as clinical symptoms such as cognitive deficits [2, 3].