Our biological studies were designed to enlighten pathological accumulation of HDAC6 in AD animal brains and how it changes over age, as well as the association between HDAC6 regulation with AD‐associated amyloid pathogenesis and pathophysiological alterations (phagocytosis, chemokines/cytokines generation or microtubule degeneration) in detail using our newly developed HDAC6i PB118[15] in the microglia BV2 cell and the 3D human neural stem cell model of AD. The gene discussed is HDAC6; the disease is amyloidosis.