Longitudinal changes of tau PET imaging in relation to hypometabolism in prodromal and Alzheimer’s disease dementia

• DOI: 10.1038/mp.2017.108
• Publication Date: 2017-05-16T08:00:53Z
• Authors: K Chiotis; L Saint-Aubert; E Rodriguez-Vieitez; A Leuzy; O Almkvist; I Savitcheva; M Jonasson; M Lubberink; A Wall; G Antoni; A Nordberg
• Keywords: Pittsburgh compound B; Prodromal Stage

The development of tau-specific positron emission tomography (PET) tracers allows imaging in vivo the regional load tau pathology Alzheimer's disease (AD) and other tauopathies. Eighteen patients with baseline investigations enroled a 17-month follow-up study, including 16 AD (10 had mild cognitive impairment positive amyloid PET scan, that is, prodromal AD, six dementia) two corticobasal syndrome. All underwent scans [18F]THK5317 (tau deposition) [18F]FDG (glucose metabolism) at follow-up, neuropsychological assessment scan [11C]PIB (amyloid-β only. At group level, (prodromal or showed unchanged retention over time, contrast to significant decreases uptake temporoparietal areas. pattern changes was heterogeneous across all patients, qualitative differences both between groups among individual patients. High significantly associated time low episodic memory encoding scores, while global cognition scores. Both syndrome negative high different distribution from homogeneous increased basal ganglia time. These findings highlight propagation symptomatic seen glucose metabolism, which better tracked clinical progression.