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Journal ArticleDOI

Neuroprotective effects of the Sigma-1 receptor (S1R) agonist PRE-084, in a mouse model of motor neuron disease not linked to SOD1 mutation.

TLDR
The results support pharmacological manipulation of S1R as a promising strategy to cure ALS and point to increased availability of growth factors and modulation of astrocytosis and of macrophage/microglia as part of the mechanisms involved in S 1R-mediated neuroprotection.
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This article is published in Neurobiology of Disease.The article was published on 2014-02-01. It has received 107 citations till now. The article focuses on the topics: Motor neuron & Neurodegeneration.

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Citations
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Compromised MAPK signaling in human diseases: an update

TL;DR: Recent research on the roles of MAPK signaling pathways in human diseases, with a focus on cancer and neurodegenerative conditions is summarized.
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Amyotrophic Lateral Sclerosis: A Focus on Disease Progression

TL;DR: The progression of the disease is discussed from the viewpoint of the potential biomarkers described to date in human and animal model samples and potential therapeutic strategies for ALS treatment and future, innovative perspectives are considered.
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The Sigma-1 Receptor as a Pluripotent Modulator in Living Systems

TL;DR: This work proposes that Sig-1R is a pluripotent modulator with resultant multiple functional manifestations in living systems and investigates its role in central nervous system diseases.
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Role of sigma-1 receptors in neurodegenerative diseases.

TL;DR: An overview of the biological mechanisms frequently associated with neurodegeneration is provided, and how sigma-1 receptors may alter these mechanisms to preserve or restore neuronal function is discussed.
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Mitochondria‐associated membrane collapse is a common pathomechanism in SIGMAR1‐ and SOD1‐linked ALS

TL;DR: The findings indicate that a loss of Sig1R function is causative for ALS16, and collapse of the MAM is a common pathomechanism in both Sig 1R‐ and SOD1‐linked ALS, and the discovery of the selective enrichment of IP3R3 in motor neurons suggests that integrity of theMAM is crucial for the selective vulnerability in ALS.
References
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Fiji: an open-source platform for biological-image analysis

TL;DR: Fiji is a distribution of the popular open-source software ImageJ focused on biological-image analysis that facilitates the transformation of new algorithms into ImageJ plugins that can be shared with end users through an integrated update system.
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Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord.

TL;DR: Together, these data suggest that polarizing the differentiation of resident microglia and infiltrating blood monocytes toward an M2 or “alternatively” activated macrophage phenotype could promote CNS repair while limiting secondary inflammatory-mediated injury.
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Sigma-1 Receptor Chaperones at the ER- Mitochondrion Interface Regulate Ca2+ Signaling and Cell Survival

TL;DR: The results reveal that the orchestrated ER chaperone machinery at MAM, by sensing ER Ca(2+) concentrations, regulates ER-mitochondrial interorganellar Ca( 2+) signaling and cell survival.
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Astrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons

TL;DR: It is shown that expression of mutated human SOD1 in primary mouse spinal motor neurons does not provoke motor neuron degeneration, and indicates that astrocytes may play a role in the specific degeneration of spinal motor neuron neurons in ALS.
Journal ArticleDOI

Non–cell autonomous toxicity in neurodegenerative disorders: ALS and beyond

TL;DR: The evidence is reviewed here the evidence that it is the convergence of damage developed within multiple cell types, including within neighboring nonneuronal supporting cells, which is crucial to neuronal dysfunction.
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