ArticleNature medicine2012
Naratriptan mitigates CGRP1-associated motor neuron degeneration caused by an expanded polyglutamine repeat tract.
Article in Nature medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Restoring early postnatal synaptic dysregulation rescues motor neuron degeneration in a mouse model of Spinal and Bulbar Muscular Atrophy.Nature communications · 2026Article
- Dysregulated synaptic gene expression in oligodendrocytes of spinal and bulbar muscular atrophy.JCI insight · 2025Article
- Label-free morphology-based phenotypic analysis of spinal and bulbar muscular atrophy muscle cell models.Disease models & mechanisms · 2025Article
- Unraveling the role of CGRP in neurological diseases: a comprehensive exploration to pathological mechanisms and therapeutic implications.Molecular biology reports · 2025Review
- Mid1 is associated with androgen-dependent axonal vulnerability of motor neurons in spinal and bulbar muscular atrophy.Cell death & disease · 2022Article
- CGRP-Mediated Prolactin Upregulation: a Possible Pathomechanism in IgG4-Related Disease.Inflammation · 2021Article
- Unveiling synapse pathology in spinal bulbar muscular atrophy by genome-wide transcriptome analysis of purified motor neurons derived from disease specific iPSCs.Molecular brain · 2020Article
- Upregulation of Extracellular Vesicles-Encapsulated miR-132 Released From Mesenchymal Stem Cells Attenuates Ischemic Neuronal Injury by Inhibiting Smad2/c-jun PathwayFrontiers in cell and developmental biology · 2020Article
- Src inhibition attenuates polyglutamine-mediated neuromuscular degeneration in spinal and bulbar muscular atrophy.Nature communications · 2019Article
- DNA methylation inhibitor attenuates polyglutamine-induced neurodegeneration by regulating Hes5.EMBO molecular medicine · 2019Article
- Gene expression analysis reveals early dysregulation of disease pathways and links Chmp7 to pathogenesis of spinal and bulbar muscular atrophy.Scientific reports · 2019Article
- Protective Effects of Calcitonin Gene-Related Peptide-Mediated p38 Mitogen-Activated Protein Kinase Pathway on Severe Acute Pancreatitis in Rats.Digestive diseases and sciences · 2019Article
- Trinucleotide Repeat Expansion Diseases, RNAi, and Cancer.Trends in cancer · 2018Review
- Correlation of insulin resistance and motor function in spinal and bulbar muscular atrophy.Journal of neurology · 2017Article
- Endoplasmic Reticulum (ER) Stress and Endocrine Disorders.International journal of molecular sciences · 2017Review
- Sphingolipid Metabolism Is Dysregulated at Transcriptomic and Metabolic Levels in the Spinal Cord of an Animal Model of Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2017Article
- Spinal and Bulbar Muscular Atrophy Overview.Journal of molecular neuroscience : MN · 2016Review
- Trinucleotide repeats and protein folding and disease: the perspective from studies with the androgen receptor.Future science OA · 2015Review
- Article
- The RhoGEF Net1 is required for normal mammary gland development.Molecular endocrinology (Baltimore, Md.) · 2014Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal and bulbar muscular atrophy (SBMA) is a motor neuron disease caused by the expansion of the CAG triplet repeat within the androgen receptor (AR) gene. Here, we demonstrated that pathogenic AR upregulates the gene encoding calcitonin gene-related peptide α (CGRP1). In neuronal cells, overexpression of CGRP1 induced cellular damage via the activation of the c-Jun N-terminal kinase (JNK) pathway, whereas pharmacological suppression of CGRP1 or JNK attenuated the neurotoxic effects of pathogenic AR. The depletion of CGRP1 inactivated JNK and suppressed neurodegeneration in a mouse model of SBMA. Naratriptan, a serotonin 1B/1D (5-hydroxytryptamine 1B/1D, or 5-HT1B/1D) receptor agonist, decreased CGRP1 expression via the induction of dual-specificity protein phosphatase 1 (DUSP1), attenuated JNK activity and mitigated pathogenic AR-mediated neuronal damage in cellular and mouse SBMA models. These observations suggest that pharmacological activation of the 5-HT1B/1D receptor may be used therapeutically to treat SBMA and other polyglutamine-related neurodegenerative diseases.
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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.