Post-mortem studies of those without dementia report the accumulation of hyperphosphorylated tau into neurofibrillary tangles, the build-up of amyloid-beta (Aβ) into plaques5,6 and the presence of GFAP (reflecting neuroinflammation).6,7 Biomarkers reflecting the pathological hallmarks of Alzheimer’s disease8-10 such as plasma phosphorylated tau 181 (p-tau181) and plasma Aβ (both Aβ40, Aβ42 and the Aβ42/40 ratio) have been investigated as biomarkers associated with cognitive function. This evidence concerns the gene MAPT and dementia.