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Longitudinal changes of tau PET imaging in relation to hypometabolism in prodromal and Alzheimer's disease dementia
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2018 (Engelska)Ingår i: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 23, nr 7, s. 1666-1673Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The development of tau-specific positron emission tomography (PET) tracers allows imaging in vivo the regional load of tau pathology in Alzheimer's disease (AD) and other tauopathies. Eighteen patients with baseline investigations enroled in a 17-month follow-up study, including 16 with AD (10 had mild cognitive impairment and a positive amyloid PET scan, that is, prodromal AD, and six had AD dementia) and two with corticobasal syndrome. All patients underwent PET scans with [(18)F]THK5317 (tau deposition) and [(18)F]FDG (glucose metabolism) at baseline and follow-up, neuropsychological assessment at baseline and follow-up and a scan with [(11)C]PIB (amyloid-β deposition) at baseline only. At a group level, patients with AD (prodromal or dementia) showed unchanged [(18)F]THK5317 retention over time, in contrast to significant decreases in [(18)F]FDG uptake in temporoparietal areas. The pattern of changes in [(18)F]THK5317 retention was heterogeneous across all patients, with qualitative differences both between the two AD groups (prodromal and dementia) and among individual patients. High [(18)F]THK5317 retention was significantly associated over time with low episodic memory encoding scores, while low [(18)F]FDG uptake was significantly associated over time with both low global cognition and episodic memory encoding scores. Both patients with corticobasal syndrome had a negative [(11)C]PIB scan, high [(18)F]THK5317 retention with a different regional distribution from that in AD, and a homogeneous pattern of increased [(18)F]THK5317 retention in the basal ganglia over time. These findings highlight the heterogeneous propagation of tau pathology among patients with symptomatic AD, in contrast to the homogeneous changes seen in glucose metabolism, which better tracked clinical progression.Molecular Psychiatry advance online publication, 16 May 2017; doi:10.1038/mp.2017.108.

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2018. Vol. 23, nr 7, s. 1666-1673
Nationell ämneskategori
Neurovetenskaper Biokemi och molekylärbiologi
Identifikatorer
URN: urn:nbn:se:uu:diva-322909DOI: 10.1038/mp.2017.108ISI: 000442358000015PubMedID: 28507319OAI: oai:DiVA.org:uu-322909DiVA, id: diva2:1103899
Forskningsfinansiär
Vetenskapsrådet, 05817Stiftelsen för strategisk forskning (SSF)Stockholms läns landstingGun och Bertil Stohnes StiftelseKarolinska Institutets ForskningsstiftelseHjärnfondenWenner-Gren StiftelsernaEU, FP7, Sjunde ramprogrammetDemensförbundetTillgänglig från: 2017-05-31 Skapad: 2017-05-31 Senast uppdaterad: 2018-11-05Bibliografiskt granskad

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Jonasson, MyLubberink, MarkWall, AndersAntoni, Gunnar

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