ArticleNeurobiology of aging2014
Orchestrated increase of dopamine and PARK mRNAs but not miR-133b in dopamine neurons in Parkinson's disease.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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.
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- MicroRNAs in Parkinson's disease: a systematic review and diagnostic accuracy meta-analysis.Scientific reports · 2023Pooled it
- Epigenetic Explorations of Neurological Disorders, the Identification Methods, and Therapeutic Avenues.International journal of molecular sciences · 2024Review
- MicroRNAs regulation in Parkinson's disease, and their potential role as diagnostic and therapeutic targets.NPJ Parkinson's disease · 2024Review
- An Overview of Epigenetic Changes in the Parkinson's Disease Brain.International journal of molecular sciences · 2024Review
- Deep learning-based image analysis identifies a DAT-negative subpopulation of dopaminergic neurons in the lateral Substantia nigra.Communications biology · 2023Article
- Dysregulated miRNAs as Biomarkers and Therapeutical Targets in Neurodegenerative Diseases.Journal of personalized medicine · 2022Review
- Parkinson's disease and microRNAs - Lessons from model organisms and human studies.Experimental gerontology · 2021Review
- Article
- Overexpression of MicroRNA-133a Inhibits Apoptosis and Autophagy in a Cell Model of Parkinson's Disease by Downregulating Ras-Related C3 Botulinum Toxin Substrate 1 (RAC1).Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Nucleic Acid-Based Therapeutics for Parkinson's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- MicroRNAs and the Genetic Nexus of Brain Aging, Neuroinflammation, Neurodegeneration, and Brain Trauma.Aging and disease · 2019Review
- MicroRNAs: Game Changers in the Regulation ofParkinson's disease · 2019Review
- NCS-1 Deficiency Affects mRNA Levels of Genes Involved in Regulation of ATP Synthesis and Mitochondrial Stress in Highly VulnerableFrontiers in molecular neuroscience · 2019Article
- Fifty-Hertz Magnetic Field Affects the Epigenetic Modulation of the miR-34b/c in Neuronal Cells.Molecular neurobiology · 2018Article
- microRNAs in Parkinson's Disease: From Pathogenesis to Novel Diagnostic and Therapeutic Approaches.International journal of molecular sciences · 2017Review
- MicroRNAs in Parkinson's disease and emerging therapeutic targets.Neural regeneration research · 2017Review
- Genetic mutations linked to Parkinson's disease differentially control nucleolar activity in pre-symptomatic mouse models.Disease models & mechanisms · 2017Article
- Sex-specific hippocampal 5-hydroxymethylcytosine is disrupted in response to acute stress.Neurobiology of disease · 2016Article
- Converging roles of ion channels, calcium, metabolic stress, and activity pattern of Substantia nigra dopaminergic neurons in health and Parkinson's disease.Journal of neurochemistry · 2016Review
- Noncoding RNA Regulation of Dopamine Signaling in Diseases of the Central Nervous System.Frontiers in molecular biosciences · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Progressive loss of substantia nigra dopamine neurons (SN DA) is a hallmark of aging and of Parkinson's disease (PD). Mutations in PARK genes cause familial PD forms. Increased expression of alpha-synuclein (PARK4) is a disease-triggering event in familial PD and also observed in SN DA neurons in sporadic PD but related transcriptional changes are unknown. With optimized single-cell quantitative real-time polymerase chain reaction analysis, we compared messenger RNA and microRNA levels in SN DA neurons from sporadic PD patients and controls. Non-optimally matched donor ages and RNA integrities are common problems when analyzing human samples. We dissected the influence of distinct ages and RNA integrities of our samples by applying a specifically-optimized, linear-mixed-effects model to quantitative real-time polymerase chain reaction-data. We identified that elevated alpha-synuclein messenger RNA levels in SN DA neurons of human PD brains were positively correlated with corresponding elevated levels of mRNAs for functional compensation of progressive SN DA loss and for enhanced proteasomal (PARK5/UCHL1) and lysosomal (PARK9/ATPase13A2) function, possibly counteracting alpha-synuclein toxicity. In contrast, microRNA miR-133b levels, previously implicated in transcriptional dysregulation in PD, were not altered in SN DA neurons in PD.
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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.