Mitochonic acid 5 alleviates amyotrophic lateral sclerosis phenotypes via mitochondrial augmentation.

doi:10.1172/jci.insight.200761

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Article

Mitochonic acid 5 alleviates amyotrophic lateral sclerosis phenotypes via mitochondrial augmentation.

JCI insight - 22 Sept 2026

Oikawa Yoshitsugu, Luo Yuhan, Suzuki Naoki, Kasahara Tomoko, Tongu Yoshiyasu, Yoshida Yuki, Tominari Tsukasa, Tanabe Shogo, Suto Yoshiko, Kashiwagi Hitomi, Saito Saki, Ikeda Kensuke, Suzuki Chitose, Kuranaga Arata, Akiyama Tetsuya, Morimoto Satoru, Aoki Yoshitsugu, Muramatsu Rieko, Soga Tomoyoshi, Aoki Masashi, Okano Hideyuki, Tanaka Tetsuhiro, Abe Takaaki, Kuranaga Erina, Toyohara Takafumi

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that urgently requires effective treatment. Mitochondrial dysfunction underlies ALS pathology and represents a potential therapeutic target. Here, we demonstrated the therapeutic potential of mitochonic acid 5 (MA-5), a novel mitochondria-targeted compound that ameliorated ALS phenotypes by enhancing mitochondrial function. In a Drosophila...

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Topics

Amyotrophic Lateral Sclerosis
Animals
Humans
Mitochondria

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Disease Models, Animal

Phenotype

Superoxide Dismutase-1

Fibroblasts

Motor Neurons

Reactive Oxygen Species

Drosophila

Induced Pluripotent Stem Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 42770300
DOI: 10.1172/jci.insight.200761
PMCID: PMC13596712

Genes

SOD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 24 Oct 2026.

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