Synaptic dysfunction induced by glycine‐alanine dipeptides in C9orf72‐ALS/FTD is rescued by SV2 replenishment

Synaptic dysfunction induced by glycine‐alanine dipeptides in C9orf72‐ALS/FTD is rescued by SV2 replenishment

Abstract The most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is an intronic hexanucleotide repeat expansion in the C9orf72 gene. In disease, RNA transcripts containing this expanded region undergo repeat‐associated non‐AUG translation to produce dipeptide r...

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Bibliographic Details
Main Authors: Brigid K Jensen, Martin H Schuldi, Kevin McAvoy, Katelyn A Russell, Ashley Boehringer, Bridget M Curran, Karthik Krishnamurthy, Xinmei Wen, Thomas Westergard, Le Ma, Aaron R Haeusler, Dieter Edbauer, Piera Pasinelli, Davide Trotti
Format: Article
Language:English
Published: Springer Nature 2020-05-01
Series:EMBO Molecular Medicine
Subjects:
amyotrophic lateral sclerosis
C9orf72
dipeptide repeat proteins
motor deficit
synaptic transmission
Online Access:https://doi.org/10.15252/emmm.201910722

Internet

https://doi.org/10.15252/emmm.201910722

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