Frontotemporal dementia (FTD) is a devastating disease where about 40% of patients have a familial history or carry an autosomal dominant mutation. Pre-symptomatic carriers offer an opportunity to study changes occurring in the brain before disease onset. Our goal was to compare FDG-PET to other imaging modalities in detecting early changes associated with MAPT genetic FTD. Participants were recruited in 5 families from the Genetic Frontotemporal Dementia Initiative (GENFI) study. Participants were all asymptomatic. Medical and neurological examination, neuropsychological and neuropsychiatric tests and several MRI imaging sequences (T1, T2, fMRI, DTI, ASL) were administered to all participants as part of the yearly GENFI follow-up. In each case, an FDG-PET scan was added to the protocol. Eighteen participants were recruited; seven were carriers of the P301L mutation on the MAPT gene. All participants were between 0–20 years before expected age of onset in their families (excepted 1 participant who was 5.5 years after expected onset and 1 participant at 29 years before onset). We generated preliminary data from a single MAPT mutation carrier using MIMNeuro (6.7). The subject was 7 years before expected onset. We found significant hypometabolism in the right amygdala (Z score = -1.71) and in both posterior cingulate gyri (Left: Z score = −1.91; Right: = -1.94) compared to 8 age-matched (±5 years) subjects from the MIMNeuro database. Structural T1 MRI was found to be normal in both these structures. Neuropsychiatric and medical examinations were normal. Neuropsychological testing was normal, except for the lexical verbal fluency test where the subject's performance was 1.60 SD below norms. We hypothesized that FDG-PET hypometabolism might be an earlier biomarker for FTD then traditional, structural imaging. This was previously shown in carriers of GRN and C9orf72 mutations, but our study is the first endeavour to explore this in MAPT mutation carriers. Whole sample analyses will be presented at the meeting.