ArticleNPJ systems biology and applications2025
MIRO1 mutation leads to metabolic maladaptation resulting in Parkinson's disease-associated dopaminergic neuron loss.
Article in NPJ systems biology and applications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Organoids: Key advances, optimization, and technological iterations in their application to neurodegenerative diseases.Neural regeneration research · 2026Article
- Review
- Rethinking PINK1/Parkin-mediated mitophagy in Parkinson's disease: functional continuity and activation-clearance uncoupling.Frontiers in aging neuroscience · 2026Review
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7 authors.
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Abstract
MIRO1 is a mitochondrial outer membrane protein important for mitochondrial distribution, dynamics and bioenergetics. Over the last decade, evidence has pointed to a link between MIRO1 and Parkinson's disease (PD) pathogenesis. Moreover, a heterozygous MIRO1 mutation (p.R272Q) was identified in a PD patient, from which an iPSC-derived midbrain organoid model was derived, showing MIRO1 mutant-dependent selective loss of dopaminergic neurons. Herein, we use patient-specific iPSC-derived midbrain organoids carrying the MIRO1 p.R272Q mutation to further explore the cellular and molecular mechanisms involved in dopaminergic neuron degeneration. Using single-cell RNA sequencing (scRNAseq) analysis and metabolic modeling we show that the MIRO1 p.R272Q mutation affects the dopaminergic neuron developmental path leading to metabolic deficits and disrupted neuron-astrocyte metabolic crosstalk, which might represent an important pathogenic mechanism leading to their loss.
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