Thirty patients with a clinical diagnosis of frontotemporal dementia underwent a baseline multi-modal imaging assessment, including [11C]PK11195 positron emission tomography (PET) to index microglial activation, and structural magnetic resonance imaging (MRI) to quantify grey-matter volume. 
PET
Thirty patients with a clinical diagnosis of frontotemporal dementia underwent a baseline multi-modal imaging assessment, including [11C]PK11195 positron emission tomography (PET) to index microglial activation, and structural magnetic resonance imaging (MRI) to quantify grey-matter volume. 
MRI
Thirty patients with a clinical diagnosis of frontotemporal dementia underwent a baseline multi-modal imaging assessment, including [11C]PK11195 positron emission tomography (PET) to index microglial activation, and structural magnetic resonance imaging (MRI) to quantify grey-matter volume.  Regional [11C]PK11195 binding potential and grey-matter volume were determined, and these were averaged within four hypothesis-driven regions of interest: bilateral frontal and temporal lobes.  Linear mixed-effect models were applied to the longitudinal cognitive test scores, with [11C]PK11195 binding potentials and grey-matter volumes as predictors of cognitive performance, with age, education and baseline cognitive performance as covariates.  When clinical diagnosis was included as a factor in the models, a significant predictive effect was found for [11C]PK11195 BPND in the left frontal lobe (-0.70, p=0.01), but not for grey-matter volumes (p>0.05), suggesting that inflammation severity in this region relates to cognitive decline regardless of clinical variant. 
PK11195
Cognition was assessed at baseline and longitudinally with the revised Addenbrooke's Cognitive Examination (ACE-R), at an average of 7-month intervals (for an average of ∼2 years, up to ∼5 years). 
ACE-R