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Article

Neuroprotection through excitability and mTOR required in ALS motoneurons to delay disease and extend survival.

Neuron - 2 Oct 2013

Saxena Smita, Roselli Francesco, Singh Katyayani, Leptien Kerstin, Julien Jean-Pierre, Gros-Louis Francois, Caroni Pico

Abstract excerpt

Delaying clinical disease onset would greatly reduce neurodegenerative disease burden, but the mechanisms influencing early preclinical progression are poorly understood. Here, we show that in mouse models of familial motoneuron (MN) disease, SOD1 mutants specifically render vulnerable MNs dependent on endogenous neuroprotection signaling involving excitability and mammalian target of rapamycin (mTOR). The most...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 24094105
DOI: 10.1016/j.neuron.2013.07.027

Genes

SOD1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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