APP and Alzheimer disease: The histopathological hallmarks of AD are extracellular Aβ plaques, resulting from pathological cleavage of the amyloid precursor protein (APP) by secretases, and intracellular neurofibrillary tangles (NFTs) of hyperphosphorylated tau (p-tau), a microtubule-associated protein.41,42 These protein aggregates are able to induce perivascular microglial activation and trigger a chronic inflammatory response which can lead to neuronal death, synaptic loss and, in turn, cognitive dysfunction.43,44