Support to this hypothesis comes from AD biomarker studies, including biomarkers of AD pathology, such as Aβ accumulation on PET imaging and in CSF; biomarkers of neurodegeneration, including biomarkers of neuronal injury and degeneration such as increased CSF tau levels and structural MRI measures of cerebral atrophy and gray matter (GM) volume; and biomarkers of synaptic dysfunction, such as lower cerebral glucose metabolism (CMRglc) on 2-deoxy-2-[18F]fluoro-d-glucose positron emission tomography (FDG PET) (Jack et al., 2013). The gene discussed is MAPT; the disease is Alzheimer disease.