ArticleFrontiers in neuroscience2019
Mutational Analysis of Sigma-1 Receptor's Role in Synaptic Stability.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Psychedelics and Neuroplasticity: A Systematic Review Unraveling the Biological Underpinnings of Psychedelics.Frontiers in psychiatry · 2021Pooled it
- Alzheimer's Disease and MERC Dysfunction: Integrating Mechanisms, Biomarkers, and Therapeutic Strategies.Molecular neurobiology · 2026Review
- Pridopidine, a Potent and Selective Therapeutic Sigma-1 Receptor (S1R) Agonist for Treating Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2025Review
- CRISPR/Cas9-Based therapeutics as a promising strategy for management of Alzheimer's disease: progress and prospects.Frontiers in cellular neuroscience · 2025Review
- CRISPR/Cas9 Gene Editing: A Novel Approach Towards Alzheimer's Disease Treatment.CNS & neurological disorders drug targets · 2024Review
- Pridopidine Promotes Synaptogenesis and Reduces Spatial Memory Deficits in the Alzheimer's Disease APP/PS1 Mouse Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Activation of the sigma-1 receptor chaperone alleviates symptoms of Wolfram syndrome in preclinical models.Science translational medicine · 2022Article
- Emerging Benefits: Pathophysiological Functions and Target Drugs of the Sigma-1 Receptor in Neurodegenerative Diseases.Molecular neurobiology · 2021Review
- Sigma-1 Receptor Is Critical for Mitochondrial Activity and Unfolded Protein Response in Larval Zebrafish.International journal of molecular sciences · 2021Article
- Involvement of Chaperone Sigma1R in the Anxiolytic Effect of Fabomotizole.International journal of molecular sciences · 2021Article
- CRISPR-Cas9: A Promising Genome Editing Therapeutic Tool for Alzheimer's Disease-A Narrative Review.Neurology and therapy · 2020Review
- The ALS-related σ1R E102Q Mutant Eludes Ligand Control and Exhibits Anomalous Response to Calcium.International journal of molecular sciences · 2020Article
- Chaperone Sigma1R and Antidepressant Effect.International journal of molecular sciences · 2020Review
- Gene Editing and Alzheimer's Disease: Is There Light at the End of the Tunnel?Frontiers in genome editing · 2020Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Sigma-1 receptor (S1R) is an endoplasmic reticulum (ER) resident transmembrane protein. In our previous experiments, we demonstrated neuroprotective effects of pridopidine, an agonist of S1R, in cellular and animal models of Huntington's disease (HD) and Alzheimer's disease (AD). Consistent with previous observations, deletion of endogenous S1R with CRISPR/Cas9 in cultured hippocampal neurons resulted in fewer mushroom-shaped dendritic spines. Overexpression of human S1R restored mushroom spine density to control levels. In contrast, overexpression of S1R with the Δ31-50 deletion (linked to distal hereditary motor neuropathy) or the E102Q mutation (linked to amyotrophic lateral sclerosis) destabilized mushroom spines. Recently a crystal structure of S1R was determined in lipidic cubic phase. In the present study, we took an advantage of this structural information and performed docking studies with pridopidine and the S1R structural model. We generated a series of S1R point mutations based on residues predicted to be involved in direct association with pridopidine. We discovered that all ligand binding-site mutants were able to compensate for loss of endogenous S1R. However, most of these mutants were not able to support pridopidine-induced rescue of mushroom spines in presenilin-1-mutant cultures. Our mutational analysis was in agreement with
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.