Today, it is broadly accepted that AD brains encompass gross neuropathology including brain atrophy and enlargement of ventricles, microscopic amyloid neuropathologies (e.g., Aβ plaques, CAA, neurofibrillary tau tangles, Lewy body α-synuclein pathology, and TDP-43 aggregates), neurovascular unit dysfunction [e.g., pericyte loss, blood-brain barrier (BBB) breakdown], and altered subcellular players (e.g., BBB transporter expression changes, post-translational modifications) (Figure 1). The gene discussed is SNCA; the disease is amyloidosis.