However, research has shifted to a multifactorial aetiology approach to AD, recognising the unique temporal contributions of (a) Aβ1-42 accumulation, formation and accumulation of toxic, soluble Aβ oligomers (AβOs); (b) the binding of zinc, copper, and iron cations to Aβ1-42 peptides that accelerates formation of AβOs; (c) tau protein phosphorylation, and (d) oxidative stress and chronic neuroinflammation elicited and sustained by glial cells. The gene discussed is MAPT; the disease is Alzheimer disease.