Current clinical diagnostics—for example CSF amyloid-β and tau measures, α-synuclein assays, neurofilament light (NfL), and neuroimaging (magnetic resonance imaging, MRI)—predominantly detect downstream proteinopathy or structural injury and commonly become abnormal only after substantial neural damage [43,48,49,50,51,52]. This evidence concerns the gene MAPT and proteostasis deficiencies.