Progressive Mitochondrial SOD1<sup>G93A</sup> Accumulation Causes Severe Structural, Metabolic and Functional Aberrations through OPA1 Down-Regulation in a Mouse Model of Amyotrophic Lateral Sclerosis

Progressive Mitochondrial SOD1<sup>G93A</sup> Accumulation Causes Severe Structural, Metabolic and Functional Aberrations through OPA1 Down-Regulation in a Mouse Model of Amyotrophic Lateral Sclerosis

In recent years, the “non-autonomous motor neuron death” hypothesis has become more consolidated behind amyotrophic lateral sclerosis (ALS). It postulates that cells other than motor neurons participate in the pathology. In fact, the involvement of the autonomic nervous system is fundamental since p...

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Bibliographic Details
Main Authors: Iago Méndez-López, Francisco J. Sancho-Bielsa, Tobias Engel, Antonio G. García, Juan Fernando Padín
Format: Article
Language:English
Published: MDPI AG 2021-07-01
Series:International Journal of Molecular Sciences
Subjects:
amyotrophic lateral sclerosis
SOD1<sup>G93A</sup>
chromaffin cell
mitochondrial dysfunction
OPA1
Online Access:https://www.mdpi.com/1422-0067/22/15/8194

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