[3] FTDP-17 is caused by mutations in the MAPT (microtubule associated protein tau) gene located on the q arm of chromosome 17, and has three cardinal features: behavioral and personality changes, cognitive impairment, and motor symptoms.

Memory, orientation, and visuospatial functions deteriorate as a result, while echolalia, palilalia, verbal and vocal perseverations develop.

FTDP-17 parkinsonism is distinguished by symmetrical bradykinesia, postural instability, rigidity affecting both axial and appendicular musculature, a lack of resting tremor, as well as poor or no response to levodopa therapy.

FTDP-17 is frequently confused with Pick's disease, sporadic progressive supranuclear palsy (PSP), or corticobasal degeneration (CBD) in the absence of a positive family history or molecular genetic data.

Other familial frontotemporal dementias, Parkinson's disease (PD), and multiple system atrophy (MSA) should be ruled out.

[2] Individual patients' and genetic kindreds' prognoses and rates of disease progression vary greatly, ranging from several months to several years, and in exceptional cases, as long as two decades.