Role of Miro1 in Mitochondrial Dysfunction and Neurodegeneration in Huntington's Disease.

Authors

Mustak Ahamed, Khadga Raj Aran

Published in

Current neurovascular research. Oct 07, 2026. Epub Oct 07, 2026.

Abstract

Huntington's Disease (HD) is an autosomal dominant neurodegenerative disorder that is caused by expansion of Cytosine-Adenine-Guanine (CAG) repeats in the Huntingtin (HTT) gene and leads to progressive motor, cognitive, and psychiatric dysfunction. Mitochondrial dysfunction is a major pathological feature of HD. Mitochondrial Rho GTPase 1 (Miro1) controls mitochondrial trafficking, calcium homeostasis, mitophagy, and neuronal signaling, and its dysregulation may contribute significantly to the progression of HD.
The literature search to identify relevant studies on Miro1 biology, mitochondrial dysfunction, mitophagy, neuroinflammation, and emerging therapeutic strategies in HD followed a narrative review of the PubMed, Scopus, ScienceDirect, and Google Scholar databases. Original research articles, review articles, and preclinical studies published in English were screened for relevance, and the retrieved evidence was critically synthesized to provide an updated overview of Miro1's role in HD pathogenesis and its therapeutic potential.
Mutant Huntingtin (mHTT) perturbs Miro1-dependent mitochondrial transport, which leads to mitochondrial mislocalization, defective mitophagy, oxidative stress, and synaptic dysfunction. Miro1 dysregulation also facilitates neuroinflammatory signaling and neuronal vulnerability. Advances in AI have led to improved early diagnosis of HD through neuroimaging and digital biomarkers. Emerging therapies targeting Miro1, including gene therapy, nanocarriers, and pharmacological modulators, show promising neuroprotective potential in preclinical models.
Miro1 is a potentially important molecular link between mitochondrial dysfunction and neurodegeneration in HD. Targeting Miro1-mediated pathways may restore mitochondrial homeostasis and may be a promising therapeutic strategy for disease modification.

PMID:
42865193
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.

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