Till sidans topp

Sidansvarig: Webbredaktion
Sidan uppdaterades: 2012-09-11 15:12

Tipsa en vän
Utskriftsversion

18F-AV-1451 tau PET imagi… - Göteborgs universitet Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

18F-AV-1451 tau PET imaging correlates strongly with tau neuropathology in MAPT mutation carriers

Artikel i vetenskaplig tidskrift
Författare R. Smith
A. Puschmann
Michael Schöll
T. Ohlsson
J. van Swieten
M. Honer
E. Englund
O. Hansson
Publicerad i Brain
Volym 139
Nummer/häfte 9
Sidor 2372-2379
ISSN 0006-8950
Publiceringsår 2016
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 2372-2379
Språk en
Länkar dx.doi.org/10.1093/brain/aww163
Ämnesord tau, frontotemporal dementia, Alzheimer's disease, positron emission tomography, MAPT R406W mutation, positron-emission-tomography, alzheimer-disease, presenile-dementia, bitemporal atrophy, r406w mutation, ftdp-17, brain, hypometabolism, patient, Neurosciences & Neurology
Ämneskategorier Neurologi

Sammanfattning

Tau positron emission tomography ligands provide the novel possibility to image tau pathologyin vivo. However, little is known about howin vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. We performed tau positron emission tomography imaging with F-18-AV-1451 in three patients harbouring a p.R406W mutation in theMAPT gene, encoding tau. This mutation results in 3- and 4-repeat tau aggregates similar to those in Alzheimer's disease, and many of the mutation carriers initially suffer from memory impairment and temporal lobe atrophy. Two patients with short disease duration and isolated memory impairment exhibited F-18-AV-1451 uptake mainly in the hippocampus and adjacent temporal lobe regions, correlating with glucose hypometabolism in corresponding regions. One patient died after 26 years of disease duration with dementia and behavioural deficits. Pre-mortem, there was F-18-AV-1451 uptake in the temporal and frontal lobes, as well as in the basal ganglia, which strongly correlated with the regional extent and amount of tau pathology in post-mortem brain sections. Amyloid-beta (F-18-flutemetamol) positron emission tomography scans were negative in all cases, as were stainings of brain sections for amyloid. This provides strong evidence that F-18-AV-1451 positron emission tomography can be used to accurately quantifyin vivo the regional distribution of hyperphosphorylated tau protein.

Sidansvarig: Webbredaktion|Sidan uppdaterades: 2012-09-11
Dela:

På Göteborgs universitet använder vi kakor (cookies) för att webbplatsen ska fungera på ett bra sätt för dig. Genom att surfa vidare godkänner du att vi använder kakor.  Vad är kakor?