It was recently well identified that loss-of-function mutations in the progranulin (PGRN) gene are the crucial etiology of frontotemporal dementia (FTD), which is the second most common dementia in people under the age of 65 after Alzheimer’s disease [49, 50], and subsequently induce FTD-like behavioral and neuropsychiatric disturbances in memory and learning cognition, social interaction, depressive-like and anxiety-like symptoms both in patients with genetic FTD [51] and in a mouse model of PGRN deficiency [38]. The gene discussed is GRN; the disease is early-onset autosomal dominant Alzheimer disease.