This is also true ofmitochondrial dysfunction and glucose hypometabolism which is apparent in theposterior cingulate cortex and other AD-vulnerable brain regions in MCI patients andhealthy adult carriers of APOE ε4 many years oreven decades before the development of clinical symptoms and, crucially, before anydiscernible evidence of tau or Aβ pathology [234, 235]; reviewedby [236]. The gene discussed is APOE; the disease is Alzheimer disease.