This is an important pointas the remainder of the paper focuses on the third research question, namely,whether differentially elevated inflammation and oxidative stress in the brain andperiphery of AD patients is sufficient to explain impaired mitochondrial function,synaptic dysfunction, PPA2 inhibition, elevated mTOR, elevated GSK-3, impairedmacro- and microautophagy, decreased proteasome function, increased ironaccumulation and transition metal dyshomeostasis reported in AD patients comparedwith age- and sex-matched controls. The gene discussed is PPA2; the disease is Alzheimer disease.