ArticlePloS one2012
Dopamine induced neurodegeneration in a PINK1 model of Parkinson's disease.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 75 citations in OpenAlex.
- Fluorescent sensors for intracellular signaling in the brain: imaging neurons, glia, and vascular cells.Neurophotonics · 2025Article
- Exploring Therapeutic Frontiers: Unveiling the Potential of Natural Diterpenoid Derivatives in Addressing Neurological Disorders.Current pharmaceutical biotechnology · 2025Review
- Cell-Permeable HSP70 Protects Neurons and Astrocytes Against Cell Death in the Rotenone-Induced and Familial Models of Parkinson's Disease.Molecular neurobiology · 2024Article
- Interplay of mitochondrial calcium signalling and reactive oxygen species production in the brain.Biochemical Society transactions · 2024Review
- Review
- Advancements in Genetic and Biochemical Insights: Unraveling the Etiopathogenesis of Neurodegeneration in Parkinson's Disease.Biomolecules · 2024Review
- Systemic Metabolism and Mitochondria in the Mechanism of Alzheimer's Disease: Finding Potential Therapeutic Targets.International journal of molecular sciences · 2023Review
- The Hidden Notes of Redox Balance in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- A review: traditional herbs and remedies impacting pathogenesis of Parkinson's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Review
- Editorial: Mitochondrial therapy in neurological diseases.Frontiers in molecular neuroscience · 2022Article
- Lactate and Pyruvate Activate Autophagy and Mitophagy that Protect Cells in Toxic Model of Parkinson's Disease.Molecular neurobiology · 2022Article
- In vivo brain imaging of mitochondrial CaBiochimica et biophysica acta. Molecular cell research · 2021Review
- Mitochondrial biogenesis as a therapeutic target for traumatic and neurodegenerative CNS diseases.Experimental neurology · 2020Review
- Mesencephalic and extramesencephalic dopaminergic systems in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- LRRK2 deficiency induced mitochondrial CaCell death & disease · 2019Article
- Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction.Neurobiology of aging · 2019Article
- Deuterated Polyunsaturated Fatty Acids Reduce Oxidative Stress and Extend the Lifespan ofFrontiers in physiology · 2019Article
- α-synuclein oligomers interact with ATP synthase and open the permeability transition pore in Parkinson's disease.Nature communications · 2018Article
- Gene-by-environment interactions that disrupt mitochondrial homeostasis cause neurodegeneration in C. elegans Parkinson's models.Cell death & disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundParkinson's disease is a common neurodegenerative disease characterised by progressive loss of dopaminergic neurons, leading to dopamine depletion in the striatum. Mutations in the PINK1 gene cause an autosomal recessive form of Parkinson's disease. Loss of PINK1 function causes mitochondrial dysfunction, increased reactive oxygen species production and calcium dysregulation, which increases susceptibility to neuronal death in Parkinson's disease. The basis of neuronal vulnerability to dopamine in Parkinson's disease is not well understood. METHODOLOGY: We investigated the mechanism of dopamine induced cell death in transgenic PINK1 knockout mouse neurons. We show that dopamine results in mitochondrial depolarisation caused by mitochondrial permeability transition pore (mPTP) opening. Dopamine-induced mPTP opening is dependent on a complex of reactive oxygen species production and calcium signalling. Dopamine-induced mPTP opening, and dopamine-induced cell death, could be prevented by inhibition of reactive oxygen species production, by provision of respiratory chain substrates, and by alteration in calcium signalling.
conclusionsThese data demonstrate the mechanism of dopamine toxicity in PINK1 deficient neurons, and suggest potential therapeutic strategies for neuroprotection in Parkinson's disease.
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Registered trials
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.