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@ARTICLE{Premi:1019087,
author = {Premi, Enrico and Pengo, Marta and Mattioli, Irene and
Cantoni, Valentina and Dukart, Jürgen and Gasparotti,
Roberto and Buratti, Emanuele and Padovani, Alessandro and
Bocchetta, Martina and Todd, Emily G. and Bouzigues,
Arabella and Cash, David M. and Convery, Rhian S. and
Russell, Lucy L. and Foster, Phoebe and Thomas, David L. and
van Swieten, John C. and Jiskoot, Lize C. and Seelaar, Harro
and Galimberti, Daniela and Sanchez-Valle, Raquel and
Laforce, Robert and Moreno, Fermin and Synofzik, Matthis and
Graff, Caroline and Masellis, Mario and Tartaglia, Maria
Carmela and Rowe, James B. and Tsvetanov, Kamen A. and
Vandenberghe, Rik and Finger, Elizabeth and Tiraboschi,
Pietro and de Mendonça, Alexandre and Santana, Isabel and
Butler, Chris R. and Ducharme, Simon and Gerhard, Alexander
and Levin, Johannes and Otto, Markus and Sorbi, Sandro and
Le Ber, Isabelle and Pasquier, Florence and Rohrer, Jonathan
D. and Borroni, Barbara and Esteve, Aitana Sogorb and
Heller, Carolin and Greaves, Caroline V. and Zetterberg,
Henrik and Swift, Imogen J. and Samra, Kiran and Shafei,
Rachelle and Timberlake, Carolyn and Cope, Thomas and
Rittman, Timothy and Arighi, Andrea and Fenoglio, Chiara and
Scarpini, Elio and Fumagalli, Giorgio and Borracci, Vittoria
and Rossi, Giacomina and Giaccone, Giorgio and Di Fede,
Giuseppe and Caroppo, Paola and Tiraboschi, Pietro and
Prioni, Sara and Redaelli, Veronica and Tang-Wai, David and
Rogaeva, Ekaterina and Castelo-Branco, Miguel and Freedman,
Morris and Keren, Ron and Black, Sandra and Mitchell, Sara
and Shoesmith, Christen and Bartha, Robart and Rademakers,
Rosa and Poos, Jackie and Papma, Janne M. and Giannini,
Lucia and van Minkelen, Rick and Pijnenburg, Yolande and
Nacmias, Benedetta and Ferrari, Camilla and Polito, Cristina
and Lombardi, Gemma and Bessi, Valentina and Veldsman,
Michele and Andersson, Christin and Thonberg, Hakan and
Öijerstedt, Linn and Jelic, Vesna and Thompson, Paul and
Langheinrich, Tobias and Lladó, Albert and Antonell, Anna
and Olives, Jaume and Balasa, Mircea and Bargalló, Nuria
and Borrego-Ecija, Sergi and Verdelho, Ana and Maruta,
Carolina and Ferreira, Catarina B. and Miltenberger, Gabriel
and do Couto, Frederico Simões and Gabilondo, Alazne and
Gorostidi, Ana and Villanua, Jorge and Cañada, Marta and
Tainta, Mikel and Zulaica, Miren and Barandiaran, Myriam and
Alves, Patricia and Bender, Benjamin and Wilke, Carlo and
Graf, Lisa and Vogels, Annick and Vandenbulcke, Mathieu and
Van Damme, Philip and Bruffaerts, Rose and Poesen, Koen and
Rosa-Neto, Pedro and Gauthier, Serge and Camuzat, Agnès and
Brice, Alexis and Bertrand, Anne and Funkiewiez, Aurélie
and Rinaldi, Daisy and Saracino, Dario and Colliot, Olivier
and Sayah, Sabrina and Prix, Catharina and Wlasich,
Elisabeth and Wagemann, Olivia and Loosli, Sandra and
Schönecker, Sonja and Hoegen, Tobias and Lombardi, Jolina
and Anderl-Straub, Sarah and Rollin, Adeline and Kuchcinski,
Gregory and Bertoux, Maxime and Lebouvier, Thibaud and
Deramecourt, Vincent and Santiago, Beatriz and Duro, Diana
and Leitão, Maria João and Almeida, Maria Rosario and
Tábuas-Pereira, Miguel and Afonso, Sónia},
title = {{E}arly neurotransmitters changes in prodromal
frontotemporal dementia: {A} {GENFI} study},
journal = {Neurobiology of disease},
volume = {179},
issn = {0969-9961},
address = {[Amsterdam]},
publisher = {Elsevier},
reportid = {FZJ-2023-05140},
pages = {106068 -},
year = {2023},
abstract = {BackgroundNeurotransmitters deficits in Frontotemporal
Dementia (FTD) are still poorly understood. Better knowledge
of neurotransmitters impairment, especially in prodromal
disease stages, might tailor symptomatic treatment
approaches.MethodsIn the present study, we applied JuSpace
toolbox, which allowed for cross-modal correlation of
Magnetic Resonance Imaging (MRI)-based measures with nuclear
imaging derived estimates covering various neurotransmitter
systems including dopaminergic, serotonergic, noradrenergic,
GABAergic and glutamatergic neurotransmission.We included
392 mutation carriers (157 GRN, 164 C9orf72, 71 MAPT),
together with 276 non-carrier cognitively healthy controls
(HC). We tested if the spatial patterns of grey matter
volume (GMV) alterations in mutation carriers (relative to
HC) are correlated with specific neurotransmitter systems in
prodromal (CDR® plus NACC FTLD = 0.5) and in symptomatic
(CDR® plus NACC FTLD≥1) FTD.ResultsIn prodromal stages of
C9orf72 disease, voxel-based brain changes were
significantly associated with spatial distribution of
dopamine and acetylcholine pathways; in prodromal MAPT
disease with dopamine and serotonin pathways, while in
prodromal GRN disease no significant findings were reported
(p < 0.05, Family Wise Error corrected). In symptomatic FTD,
a widespread involvement of dopamine, serotonin, glutamate
and acetylcholine pathways across all genetic subtypes was
found. Social cognition scores, loss of empathy and poor
response to emotional cues were found to correlate with the
strength of GMV colocalization of dopamine and serotonin
pathways (all p < 0.01).ConclusionsThis study, indirectly
assessing neurotransmitter deficits in monogenic FTD,
provides novel insight into disease mechanisms and might
suggest potential therapeutic targets to counteract
disease-related symptoms.},
cin = {INM-7},
ddc = {570},
cid = {I:(DE-Juel1)INM-7-20090406},
pnm = {5252 - Brain Dysfunction and Plasticity (POF4-525)},
pid = {G:(DE-HGF)POF4-5252},
typ = {PUB:(DE-HGF)16},
pubmed = {36898614},
UT = {WOS:000956609800001},
doi = {10.1016/j.nbd.2023.106068},
url = {https://juser.fz-juelich.de/record/1019087},
}