Perspectives in Molecular Imaging Using Staging Biomarkers and Immunotherapies in Alzheimer’s Disease

Figure 3

An hypothetical model showing the influence of genes, other diseases, and cognitive capacity on normal aging brain structure: C0 = CSF Aβ42, Tau or p-tau with brain structure in individuals typically observed without genetic and innate factors; C1 = CSF Aβ42, Tau or p-tau with brain structure in individuals typically observed with genetic risk loci (e.g., ApoE4) and/or together with comorbidity (e.g., cerebrovascular disease, cortical Lewy bodies, and frontal damage); C2 = CSF Aβ42, Tau, or p-tau with brain structure in individuals typically observed with high cognitive reserve or protective genetic loci (e.g., ApoE2); Pr−, Pr+, E−, E+, L−, and L+ = shifts early and late during preclinical, early, and late mild cognitive impairment stages. This modify illustration is adapted from figures in [91, 151–153].