ArticleNeurobiology of aging2019
Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction.
Article in Neurobiology of aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Mitophagy in neuronal health and disease: from mechanisms to neurodegeneration.The Journal of clinical investigation · 2026Review
- Loss of PINK1 causes age-dependent mitochondrial trafficking deficits in nigrostriatal dopaminergic neurons via aberrant p38 MAPK activation.NPJ Parkinson's disease · 2026Article
- The Human LRRK2-R1441G Mutation Drives Age-Dependent Oxidative Stress and Mitochondrial Dysfunction in Dopaminergic Neurons.Research square · 2025Article
- Neuroinflammatory Mechanisms and Vocalization Biomarkers in theMedical research archives · 2025Article
- Targeting ATAD3A Phosphorylation Mediated by TBK1 Ameliorates Senescence-Associated Pathologies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mitochondrion-based organellar therapies for central nervous system diseases.Cell communication and signaling : CCS · 2024Review
- PINK1-PTEN axis promotes metastasis and chemoresistance in ovarian cancer via non-canonical pathway.Journal of experimental & clinical cancer research : CR · 2023Article
- Impaired dopamine release in Parkinson's disease.Brain : a journal of neurology · 2023Review
- Mitochondrial Bioenergy in Neurodegenerative Disease: Huntington and Parkinson.International journal of molecular sciences · 2023Review
- Review
- On the Chemical and Biological Characteristics of Multifunctional Compounds for the Treatment of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Cogs in the autophagic machine-equipped to combat dementia-prone neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Endogenous PTEN-Induced Kinase 1 Regulates Dendritic Architecture and Spinogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Pink1/Parkin-Mediated Mitophagy Regulated the Apoptosis of Dendritic Cells in Sepsis.Inflammation · 2022Article
- Hepatic Mitochondrial Dysfunction and Risk of Liver Disease in an Ovine Model of "PCOS Males".Biomedicines · 2022Article
- Role of the mtDNA Mutations and Mitophagy in Inflammaging.International journal of molecular sciences · 2022Review
- Establishing Equivalent Aerobic Exercise Parameters Between Early-Stage Parkinson's Disease and Pink1 Knockout Rats.Journal of Parkinson's disease · 2022Article
- Intraperitoneal Administration of Forskolin Reverses Motor Symptoms and Loss of Midbrain Dopamine Neurons in PINK1 Knockout Rats.Journal of Parkinson's disease · 2022Article
- Review
- New insights into mitophagy and stem cells.Stem cell research & therapy · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Mutations and deletions in PTEN-induced kinase 1 (PINK1) cause autosomal recessive Parkinson's disease (PD), the second most common neurodegenerative disorder. PINK1 is a nuclear-genome encoded Ser/Thr kinase in mitochondria. PINK1 deletion was reported to affect dopamine (DA) levels in the striatum and mitochondrial functions but with conflicting results. The role of PINK1 in mitochondrial function and in PD pathogenesis remains to be elucidated thoroughly. In this study, we measured DA release using fast-scan cyclic voltammetry in acute striatal slices from both PINK1 knockout (KO) and wild-type (WT) mice at different ages. We found that single pulse-evoked DA release in the dorsal striatum of PINK1 KO mice was decreased in an age-dependent manner. Furthermore, the decrease was because of less DA release instead of an alteration of DA transporter function or DA terminal degeneration. We also found that PINK1 KO striatal slices had significantly lower basal mitochondria respiration compared with that of WT controls, and this impairment was also age-dependent. These results suggest that the impaired DA release is most likely because of mitochondrial dysfunction and lower ATP production.
Indexed as
Identifiers
What OpenQuestion holds
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.