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Naratriptan mitigates CGRP1-associated motor neuron degeneration caused by an expanded polyglutamine repeat tract.

Author: AdachiHiroaki, DoiHideki, FujiokaYusuke, IidaMadoka, IshigakiShinsuke, KatsunoMasahisa, KondoNaohide, KuriharaHiroki, MatsumotoShinjiro, MinamiyamaMakoto, MiyazakiYu, SobueGen, TanakaFumiaki

Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.
Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.

Overview

This study investigated the role of calcitonin gene-related peptide α (CGRP1) in spinal and bulbar muscular atrophy (SBMA). The results showed that pathogenic androgen receptor (AR) upregulates CGRP1 expression, which contributes to neuronal damage. Pharmacological suppression of CGRP1 or the c-Jun N-terminal kinase (JNK) pathway attenuated the neurotoxic effects of pathogenic AR.
Paper Details　
Original Abstract of the Article :
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, overexpre...See full text at original site
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引用元：
https://doi.org/10.1038/nm.2932

データ提供：米国国立医学図書館（NLM）

Naratriptan mitigates CGRP1-associated motor neuron degeneration caused by an expanded polyglutamine repeat tract

Spinal and bulbar muscular atrophy (SBMA), a debilitating motor neuron disease, is caused by a genetic mutation that disrupts the function of the androgen receptor. This study investigates the role of calcitonin gene-related peptide α (CGRP1) in SBMA and explores the potential of naratriptan, a serotonin receptor agonist, as a therapeutic agent.

A Novel Approach to Treating SBMA: Targeting CGRP1

The study found that pathogenic androgen receptors upregulate CGRP1, leading to motor neuron degeneration. Furthermore, naratriptan was shown to mitigate this neurodegeneration by reducing CGRP1 expression and attenuating the activity of the JNK pathway, a key signaling pathway involved in neuronal damage. These findings offer a promising new approach to treating SBMA, targeting a specific molecular pathway that contributes to the disease process.

Hope for Individuals with SBMA: A Potential Therapeutic Breakthrough

This research opens up exciting new possibilities for treating SBMA, a debilitating condition that currently lacks effective treatments. While further research is needed to confirm the efficacy and safety of naratriptan in human patients, these findings provide a glimmer of hope for individuals battling this disease. It's a testament to the power of scientific inquiry to discover new avenues for treating complex neurological conditions.

Dr. Camel's Conclusion

This study offers a compelling new strategy for treating SBMA, a devastating motor neuron disease. By targeting CGRP1 and its role in neurodegeneration, researchers have identified a promising therapeutic target. As a camel, I know the importance of maintaining a strong and flexible spine for navigating challenging terrains. This research holds the potential to alleviate the suffering of individuals with SBMA, offering hope for a future where this debilitating condition is no longer a burden.

Date :
  1. Date Completed 2013-01-09
  2. Date Revised 2021-10-21
Further Info :

Pubmed ID

23023499

DOI: Digital Object Identifier

10.1038/nm.2932

Related Literature

Article Analysis
・Effects of naratriptan
SNS
PICO Info
in preparation
Languages

English

Positive IndicatorAn AI analysis index that serves as a benchmark for how positive the results of the study are. Note that it is a benchmark and requires careful interpretation and consideration of different perspectives.

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