Additionally, additional research should evaluate whether there may be a dose–response effect on inflammation, oxidative stress, markers of Alzheimer’s disease progression (e.g., amyloid-β (Aβ) pathway (A), tau-mediated pathophysiology (T), and neurodegeneration (N) or AT/N classifications) [121], structural and functional neuroimaging, and cognitive function in younger and older populations with and without perceived or medically treated cognitive impairment, as well as how risk factors to MCI and cognitive neurodegeneration diseases may affect the results. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.