ArticleNPJ systems biology and applications2020
Mitochondria interaction networks show altered topological patterns in Parkinson's disease.
Article in NPJ systems biology and applications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 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
5 citing papers in PubMed.
- Gastrointestinal mucosal biopsies in Parkinson's disease: beyond alpha-synuclein detection.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Gene Therapeutic Approaches for the Treatment of Mitochondrial Dysfunction in Parkinson's Disease.Genes · 2021Review
- Gene-corrected p.A30P SNCA patient-derived isogenic neurons rescue neuronal branching and function.Scientific reports · 2021Article
- Mitochondrial and Clearance Impairment in p.D620N VPS35 Patient-Derived Neurons.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Advancing Personalized Medicine in Common Forms of Parkinson's Disease through Genetics: Current Therapeutics and the Future of Individualized Management.Journal of personalized medicine · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is linked to pathogenesis of Parkinson's disease (PD). However, individual mitochondria-based analyses do not show a uniform feature in PD patients. Since mitochondria interact with each other, we hypothesize that PD-related features might exist in topological patterns of mitochondria interaction networks (MINs). Here we show that MINs formed nonclassical scale-free supernetworks in colonic ganglia both from healthy controls and PD patients; however, altered network topological patterns were observed in PD patients. These patterns were highly correlated with PD clinical scores and a machine-learning approach based on the MIN features alone accurately distinguished between patients and controls with an area-under-curve value of 0.989. The MINs of midbrain dopaminergic neurons (mDANs) derived from several genetic PD patients also displayed specific changes. CRISPR/CAS9-based genome correction of alpha-synuclein point mutations reversed the changes in MINs of mDANs. Our organelle-interaction network analysis opens another critical dimension for a deeper characterization of various complex diseases with mitochondrial dysregulation.
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