FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations

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FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations. / Diehl-Schmid, Janine; Licata, Abigail; Goldhardt, Oliver; Förstl, Hans; Yakushew, Igor; Otto, Markus; Anderl-Straub, Sarah; Beer, Ambros; Ludolph, Albert Christian; Landwehrmeyer, Georg Bernhard; Levin, Johannes; Danek, Adrian; Fliessbach, Klaus; Spottke, Annika; Fassbender, Klaus; Lyros, Epameinondas; Prudlo, Johannes; Krause, Bernd Joachim; Volk, Alexander; Edbauer, Dieter; Schroeter, Matthias Leopold; Drzezga, Alexander; Kornhuber, Johannes; Lauer, Martin; FTLDc Study Group; Grimmer, Timo.

In: TRANSL PSYCHIAT, Vol. 9, No. 1, 31.01.2019, p. 54.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Diehl-Schmid, J, Licata, A, Goldhardt, O, Förstl, H, Yakushew, I, Otto, M, Anderl-Straub, S, Beer, A, Ludolph, AC, Landwehrmeyer, GB, Levin, J, Danek, A, Fliessbach, K, Spottke, A, Fassbender, K, Lyros, E, Prudlo, J, Krause, BJ, Volk, A, Edbauer, D, Schroeter, ML, Drzezga, A, Kornhuber, J, Lauer, M, FTLDc Study Group & Grimmer, T 2019, 'FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations', TRANSL PSYCHIAT, vol. 9, no. 1, pp. 54. https://doi.org/10.1038/s41398-019-0381-1

APA

Diehl-Schmid, J., Licata, A., Goldhardt, O., Förstl, H., Yakushew, I., Otto, M., Anderl-Straub, S., Beer, A., Ludolph, A. C., Landwehrmeyer, G. B., Levin, J., Danek, A., Fliessbach, K., Spottke, A., Fassbender, K., Lyros, E., Prudlo, J., Krause, B. J., Volk, A., ... Grimmer, T. (2019). FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations. TRANSL PSYCHIAT, 9(1), 54. https://doi.org/10.1038/s41398-019-0381-1

Vancouver

Bibtex

@article{26c14b3a76bd44d4bda51404655871f2,
title = "FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations",
abstract = "C9ORF72 mutations are the most common cause of familial frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). MRI studies have investigated structural changes in C9ORF72-associated FTLD (C9FTLD) and provided first insights about a prominent involvement of the thalamus and the cerebellum. Our multicenter, 18F-fluorodeoxyglucose positron-emission tomography study of 22 mutation carriers with FTLD, 22 matched non-carriers with FTLD, and 23 cognitively healthy controls provided valuable insights into functional changes in C9FTLD: compared to non-carriers, mutation carriers showed a significant reduction of glucose metabolism in both thalami, underscoring the key role of the thalamus in C9FTLD. Thalamic metabolism did not correlate with disease severity, duration of disease, or the presence of psychotic symptoms. Against our expectations we could not demonstrate a cerebellar hypometabolism in carriers or non-carriers. Future imaging and neuropathological studies in large patient cohorts are required to further elucidate the central role of the thalamus in C9FTLD.",
keywords = "Journal Article",
author = "Janine Diehl-Schmid and Abigail Licata and Oliver Goldhardt and Hans F{\"o}rstl and Igor Yakushew and Markus Otto and Sarah Anderl-Straub and Ambros Beer and Ludolph, {Albert Christian} and Landwehrmeyer, {Georg Bernhard} and Johannes Levin and Adrian Danek and Klaus Fliessbach and Annika Spottke and Klaus Fassbender and Epameinondas Lyros and Johannes Prudlo and Krause, {Bernd Joachim} and Alexander Volk and Dieter Edbauer and Schroeter, {Matthias Leopold} and Alexander Drzezga and Johannes Kornhuber and Martin Lauer and {FTLDc Study Group} and Timo Grimmer and Holger Jahn",
year = "2019",
month = jan,
day = "31",
doi = "10.1038/s41398-019-0381-1",
language = "English",
volume = "9",
pages = "54",
journal = "TRANSL PSYCHIAT",
issn = "2158-3188",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations

AU - Diehl-Schmid, Janine

AU - Licata, Abigail

AU - Goldhardt, Oliver

AU - Förstl, Hans

AU - Yakushew, Igor

AU - Otto, Markus

AU - Anderl-Straub, Sarah

AU - Beer, Ambros

AU - Ludolph, Albert Christian

AU - Landwehrmeyer, Georg Bernhard

AU - Levin, Johannes

AU - Danek, Adrian

AU - Fliessbach, Klaus

AU - Spottke, Annika

AU - Fassbender, Klaus

AU - Lyros, Epameinondas

AU - Prudlo, Johannes

AU - Krause, Bernd Joachim

AU - Volk, Alexander

AU - Edbauer, Dieter

AU - Schroeter, Matthias Leopold

AU - Drzezga, Alexander

AU - Kornhuber, Johannes

AU - Lauer, Martin

AU - FTLDc Study Group

AU - Grimmer, Timo

AU - Jahn, Holger

PY - 2019/1/31

Y1 - 2019/1/31

N2 - C9ORF72 mutations are the most common cause of familial frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). MRI studies have investigated structural changes in C9ORF72-associated FTLD (C9FTLD) and provided first insights about a prominent involvement of the thalamus and the cerebellum. Our multicenter, 18F-fluorodeoxyglucose positron-emission tomography study of 22 mutation carriers with FTLD, 22 matched non-carriers with FTLD, and 23 cognitively healthy controls provided valuable insights into functional changes in C9FTLD: compared to non-carriers, mutation carriers showed a significant reduction of glucose metabolism in both thalami, underscoring the key role of the thalamus in C9FTLD. Thalamic metabolism did not correlate with disease severity, duration of disease, or the presence of psychotic symptoms. Against our expectations we could not demonstrate a cerebellar hypometabolism in carriers or non-carriers. Future imaging and neuropathological studies in large patient cohorts are required to further elucidate the central role of the thalamus in C9FTLD.

AB - C9ORF72 mutations are the most common cause of familial frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). MRI studies have investigated structural changes in C9ORF72-associated FTLD (C9FTLD) and provided first insights about a prominent involvement of the thalamus and the cerebellum. Our multicenter, 18F-fluorodeoxyglucose positron-emission tomography study of 22 mutation carriers with FTLD, 22 matched non-carriers with FTLD, and 23 cognitively healthy controls provided valuable insights into functional changes in C9FTLD: compared to non-carriers, mutation carriers showed a significant reduction of glucose metabolism in both thalami, underscoring the key role of the thalamus in C9FTLD. Thalamic metabolism did not correlate with disease severity, duration of disease, or the presence of psychotic symptoms. Against our expectations we could not demonstrate a cerebellar hypometabolism in carriers or non-carriers. Future imaging and neuropathological studies in large patient cohorts are required to further elucidate the central role of the thalamus in C9FTLD.

KW - Journal Article

U2 - 10.1038/s41398-019-0381-1

DO - 10.1038/s41398-019-0381-1

M3 - SCORING: Journal article

C2 - 30705258

VL - 9

SP - 54

JO - TRANSL PSYCHIAT

JF - TRANSL PSYCHIAT

SN - 2158-3188

IS - 1

ER -