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@ARTICLE{Czuppa:164645,
author = {Czuppa, Mareike and Dhingra, Ashutosh and Zhou, Qihui and
Schludi, Carina and Koenig, Laura and Scharf, Elisabeth and
Farny, Daniel and Dalmia, Anupriya and Täger, Joachim and
Castillo Lizardo, Melissa Gissel and Katona, Eszter and
Mori, Kohji and Aumer, Tina and Schelter, Florian and
Müller, Markus and Carell, Thomas and Kalliokoski, Tuomo
and Messinger, Josef and Rizzu, Patrizia and Heutink, Peter
and Edbauer, Dieter},
title = {{D}rug screen in i{PSC}-{N}eurons identifies nucleoside
analogs as inhibitors of ({G}4{C}2)n expression in {C}9orf72
{ALS}/{FTD}},
journal = {Cell reports},
volume = {39},
number = {10},
issn = {2211-1247},
address = {[New York, NY]},
publisher = {Elsevier},
reportid = {DZNE-2022-01175},
pages = {110913},
year = {2022},
note = {(CC BY-NC-ND)},
abstract = {An intronic (G4C2)n expansion in C9orf72 causes amyotrophic
lateral sclerosis and frontotemporal dementia primarily
through gain-of-function mechanisms: the accumulation of
sense and antisense repeat RNA foci and dipeptide repeat
(DPR) proteins (poly-GA/GP/GR/PA/PR) translated from repeat
RNA. To therapeutically block this pathway, we screen a
library of 1,430 approved drugs and known bioactive
compounds in patient-derived induced pluripotent stem
cell-derived neurons (iPSC-Neurons) for inhibitors of DPR
expression. The clinically used guanosine/cytidine analogs
decitabine, entecavir, and nelarabine reduce poly-GA/GP
expression, with decitabine being the most potent. Hit
compounds nearly abolish sense and antisense RNA foci and
reduce expression of the repeat-containing nascent C9orf72
RNA transcript and its mature mRNA with minimal effects on
global gene expression, suggesting that they specifically
act on repeat transcription. Importantly, decitabine
treatment reduces (G4C2)n foci and DPRs in C9orf72 BAC
transgenic mice. Our findings suggest that nucleoside
analogs are a promising compound class for therapeutic
development in C9orf72 repeat-expansion-associated
disorders.},
keywords = {Amyotrophic Lateral Sclerosis: drug therapy / Amyotrophic
Lateral Sclerosis: genetics / Amyotrophic Lateral Sclerosis:
metabolism / Animals / C9orf72 Protein: genetics / C9orf72
Protein: metabolism / DNA Repeat Expansion / Decitabine:
metabolism / Dipeptides: metabolism / Frontotemporal
Dementia: genetics / Humans / Induced Pluripotent Stem
Cells: metabolism / Mice / Neurons: metabolism /
Nucleosides: metabolism / RNA, Antisense: metabolism},
cin = {AG Edbauer / AG Heutink 1 / München common / AG Rizzu / AG
Zhou},
ddc = {610},
cid = {I:(DE-2719)1110004 / I:(DE-2719)1210002 /
I:(DE-2719)6000016 / I:(DE-2719)1210009 /
I:(DE-2719)5000080},
pnm = {352 - Disease Mechanisms (POF4-352) / 354 - Disease
Prevention and Healthy Aging (POF4-354)},
pid = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-354},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35675776},
doi = {10.1016/j.celrep.2022.110913},
url = {https://pub.dzne.de/record/164645},
}