ArticleScientific reports2017
Conditional deletion of Ndufs4 in dopaminergic neurons promotes Parkinson's disease-like non-motor symptoms without loss of dopamine neurons.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- A human lysosomal storage disorder toolkit for decoding proteome landscapes in cortical-like and dopaminergic-like induced neurons.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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- Proteome Landscapes Decode Organelle Vulnerabilities in cortical and dopaminergic-like induced neurons Across Lysosomal Storage Disorders.bioRxiv : the preprint server for biology · 2025Article
- [Recent advances on the role of exosomes in neurodegenerative diseases].Se pu = Chinese journal of chromatography · 2025Review
- Development of an anti-tauopathy mucosal vaccine specifically targeting pathologic conformers.NPJ vaccines · 2024Article
- Oral Administration of Probiotic Bacteria Alleviates Tau Phosphorylation, Aβ Accumulation, Microglia Activation, and Memory Loss in 5xFAD Mice.Brain sciences · 2024Article
- Article
- On the Chemical and Biological Characteristics of Multifunctional Compounds for the Treatment of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- A genome on shaky ground: exploring the impact of mitochondrial DNA integrity on Parkinson's disease by highlighting the use of cybrid models.Cellular and molecular life sciences : CMLS · 2022Review
- Ndufs4 knockout mouse models of Leigh syndrome: pathophysiology and intervention.Brain : a journal of neurology · 2022Review
- Trophoblast glycoprotein is a new candidate gene for Parkinson's disease.NPJ Parkinson's disease · 2021Article
- Is there a special relationship between complex I activity and nigral neuronal loss in Parkinson's disease? A critical reappraisal.Brain research · 2021Review
- Electrochemical Detection of Dopamine at FeMolecules (Basel, Switzerland) · 2021Article
- Ndufs4 ablation decreases synaptophysin expression in hippocampus.Scientific reports · 2021Article
- Plasmodium berghei-induced malaria decreases pain sensitivity in mice.The Onderstepoort journal of veterinary research · 2021Article
- Experimental Models of Cognitive Impairment for Use in Parkinson's Disease Research: The Distance Between Reality and Ideal.Frontiers in aging neuroscience · 2021Review
- Calcium, Bioenergetics, and Parkinson's Disease.Cells · 2020Review
- A multi-faceted genotoxic network of alpha-synuclein in the nucleus and mitochondria of dopaminergic neurons in Parkinson's disease: Emerging concepts and challenges.Progress in neurobiology · 2020Review
- An ultra-stable cytoplasmic antibody engineered for in vivo applications.Nature communications · 2020Article
- Article
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Reduction of mitochondrial complex I activity is one of the major hypotheses for dopaminergic neuron death in Parkinson's disease. However, reduction of complex I activity in all cells or selectively in dopaminergic neurons via conditional deletion of the Ndufs4 gene, a subunit of the mitochondrial complex I, does not cause dopaminergic neuron death or motor impairment. Here, we investigated the effect of reduced complex I activity on non-motor symptoms associated with Parkinson's disease using conditional knockout (cKO) mice in which Ndufs4 was selectively deleted in dopaminergic neurons (Ndufs4 cKO). This conditional deletion of Ndufs4, which reduces complex I activity in dopamine neurons, did not cause a significant loss of dopaminergic neurons in substantia nigra pars compacta (SNpc), and there was no loss of dopaminergic neurites in striatum or amygdala. However, Ndufs4 cKO mice had a reduced amount of dopamine in the brain compared to control mice. Furthermore, even though motor behavior were not affected, Ndufs4 cKO mice showed non-motor symptoms experienced by many Parkinson's disease patients including impaired cognitive function and increased anxiety-like behavior. These data suggest that mitochondrial complex I dysfunction in dopaminergic neurons promotes non-motor symptoms of Parkinson's disease and reduces dopamine content in the absence of dopamine neuron loss.
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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.