Vps35 or Vps26 deficient animals display partial AD and PD-relevant neuropathologic deficits, including increased β-amyloid (Aβ) in the hippocampus [12, 13], (a major culprit of AD), and elevated α-synuclein with reduced dopamine neurons in the substantia nigra [14–20] (both PD-linked neuropathologic deficits). The gene discussed is VPS26A; the disease is Parkinson disease.