ArticleStem cell reports2019
Neural Stem Cells of Parkinson's Disease Patients Exhibit Aberrant Mitochondrial Morphology and Functionality.
Article in Stem cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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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
63 citing papers in PubMed, 93 citations in OpenAlex.
- VPS35 mutation inhibits PINK1/parkin-mediated mitophagy via increased LRRK2 kinase activity.Brain : a journal of neurology · 2026Article
- Convergent transcriptomic signature in iPSC-dopaminergic neurons of hereditary Parkinson's disease.Life science alliance · 2026Article
- Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026Review
- LRRK2 I1371V Mutation Drives Astrocytic Glucose Metabolism Failure and Induces Integrated ER-Mitochondria-Lysosome Dysfunction in Parkinson's Disease.International journal of molecular sciences · 2026Article
- Role of LRRK2 in physiological activities, diseases, and therapy.Chinese medical journal · 2026Review
- Are neurodegenerative diseases late-onset neurodevelopmental disorders? Tracing the developmental origins of neuronal vulnerability.Frontiers in neuroscience · 2026Review
- Dynamic gene regulatory network inference from single-cell data using optimal transport.Bioinformatics (Oxford, England) · 2025Article
- Immune cell metabolic dysfunction in Parkinson's disease.Molecular neurodegeneration · 2025Review
- Developmental disruption of the mitochondrial fission gene drp-1 extends the longevity of daf-2 insulin/IGF-1 receptor mutant.GeroScience · 2025Article
- Role of mitochondrial quality control in neurodegenerative disease progression.Frontiers in cellular neuroscience · 2025Review
- Review
- Evaluating chemical effects on human neural cells through calcium imaging and deep learning.iScience · 2024Article
- Loss of mitochondrial CaCell communication and signaling : CCS · 2024Article
- Engineering 3D Scaffold-Free Nanoparticle-Laden Stem Cell Constructs for Piezoelectric Enhancement of Human Neural Tissue Formation and Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Biosensors; a novel concept in real-time detection of autophagy.Biosensors & bioelectronics · 2024Review
- Quantifying nanoscopic alterations associated with mitochondrial dysfunction using three-dimensional single-molecule localization microscopy.Biomedical optics express · 2024Article
- Omics data integration suggests a potential idiopathic Parkinson's disease signature.Communications biology · 2023Article
- YKL-40 and the Cellular Metabolic Profile in Parkinson's Disease.International journal of molecular sciences · 2023Article
- Article
- Mitochondrial dysfunction and mitophagy defects in LRRK2-R1441C Parkinson's disease models.Human molecular genetics · 2023Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that Parkinson's disease (PD), besides being an age-associated disorder, might also have a neurodevelopment component. Disruption of mitochondrial homeostasis has been highlighted as a crucial cofactor in its etiology. Here, we show that PD patient-specific human neuroepithelial stem cells (NESCs), carrying the LRRK2-G2019S mutation, recapitulate key mitochondrial defects previously described only in differentiated dopaminergic neurons. By combining high-content imaging approaches, 3D image analysis, and functional mitochondrial readouts we show that LRRK2-G2019S mutation causes aberrations in mitochondrial morphology and functionality compared with isogenic controls. LRRK2-G2019S NESCs display an increased number of mitochondria compared with isogenic control lines. However, these mitochondria are more fragmented and exhibit decreased membrane potential. Functional alterations in LRRK2-G2019S cultures are also accompanied by a reduced mitophagic clearance via lysosomes. These findings support the hypothesis that preceding mitochondrial developmental defects contribute to the manifestation of the PD pathology later in life.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.