The neuroprotective effects of activated α7 nicotinic acetylcholine receptor against mutant copper-zinc superoxide dismutase 1-mediated toxicity.
AMP-Activated Protein Kinases
/ metabolism
Autophagy
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
/ metabolism
Calcium
/ metabolism
Humans
Intracellular Space
Lysosomes
/ metabolism
Mutation
Neurodegenerative Diseases
/ etiology
Neurons
/ metabolism
Neuroprotective Agents
Protein Aggregates
Protein Binding
Protein Transport
Signal Transduction
Superoxide Dismutase-1
/ genetics
TOR Serine-Threonine Kinases
/ metabolism
alpha7 Nicotinic Acetylcholine Receptor
/ agonists
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
17 12 2020
17 12 2020
Historique:
received:
29
07
2020
accepted:
02
12
2020
entrez:
18
12
2020
pubmed:
19
12
2020
medline:
11
5
2021
Statut:
epublish
Résumé
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective and progressive loss of motor neurons. Although many drugs have entered clinical trials, few have shown effectiveness in the treatment of ALS. Other studies have shown that the stimulation of α7 nicotinic acetylcholine receptor (nAChR) can have neuroprotective effects in some models of neurodegenerative disease, as well as prevent glutamate-induced motor neuronal death. However, the effect of α7 nAChR agonists on ALS-associated mutant copper-zinc superoxide dismutase 1 (SOD1) aggregates in motor neurons remains unclear. In the present study, we examined whether α7 nAChR activation had a neuroprotective effect against SOD1
Identifiants
pubmed: 33335227
doi: 10.1038/s41598-020-79189-y
pii: 10.1038/s41598-020-79189-y
pmc: PMC7746719
doi:
Substances chimiques
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
0
Neuroprotective Agents
0
Protein Aggregates
0
TFEB protein, human
0
alpha7 Nicotinic Acetylcholine Receptor
0
Superoxide Dismutase-1
EC 1.15.1.1
TOR Serine-Threonine Kinases
EC 2.7.11.1
AMP-Activated Protein Kinases
EC 2.7.11.31
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
22157Références
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