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The subtypes of PPA are differentiated by specific types of speech or language deficits.

The three PPA subtypes are the semantic, non-fluent, and logopenic variants (19).

Although psychotic symptoms such as hallucinations and delusions are rare in bv FTD, cases of these symptoms have been reported (17), particularly in patients carrying the chromosome 9 open reading frame 72 (C9orf72) repeat expansion (18).

Patients with PPA exhibit a progressive decline in linguistic skills during the early phase of the disease.

Finally, PSP-S is characterized by atypical parkinsonism with axial and symmetrical rigidity, supranuclear gaze palsy (most prominent in the vertical plane), decreased saccadic velocity, early postural instability with falls, and prominent frontal lobe dysfunction (25, 26).

Taken together, the vast heterogeneity and overlap of clinical phenotypes in FTD often poses diagnostic challenges for clinicians, in particular the presenting psychiatric symptoms that may easily be mistaken for psychiatric disorders.

Patients tend to exhibit motor speech disorders characterized by a slow speech rate, abnormal prosody, and distorted sound substitutions, additions, repetitions, and prolongations, which are occasionally accompanied by groping, trial-and-error articulatory movements (21), or agrammatic errors.

The disease may exhibit similar characteristics to many psychiatric disorders owing to its prominent behavioral features.

The concept of precision medicine has recently emerged, and it involves neurodegenerative disease treatment that is personalized to match an individual's specific pattern of neuroimaging, neuropathology, and genetic variability.

In this paper, the pathophysiology underlying FTD, which is characterized by the selective degeneration of the frontal and temporal cortices, is reviewed.

We also discuss recent advancements in FTD research from the perspectives of clinical, imaging, molecular characterizations, and treatment.

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