ReviewCellular and molecular neurobiology2001
Is there a rationale for neuroprotection against dopamine toxicity in Parkinson's disease?
Review in Cellular and molecular neurobiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- When Pathways Converge: Iron, Lipid Peroxidation, and α-Synuclein in Ferroptosis-Driven Dopaminergic Neurodegeneration.Journal of neurochemistry · 2026Review
- Dopamine modification of glycolytic enzymes impairs glycolysis: possible implications for Parkinson's disease.Cell communication and signaling : CCS · 2024Article
- Combined and sequential effects of alcohol and methamphetamine in animal models.Neuroscience and biobehavioral reviews · 2021Review
- Insights into the Pathogenesis of Neurodegenerative Diseases: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2021Review
- Genetic elimination of dopamine vesicular stocks in the nigrostriatal pathway replicates Parkinson's disease motor symptoms without neuronal degeneration in adult mice.Scientific reports · 2017Article
- Differences in vulnerability of neurons and astrocytes to heme oxygenase-1 modulation: Implications for mitochondrial ferritin.Scientific reports · 2016Article
- Pathogenesis-targeted, disease-modifying therapies in Parkinson disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014Review
- Pituitary adenylate cyclase activating polypeptide modulates catecholamine storage and exocytosis in PC12 cells.PloS one · 2014Article
- Compromising σ-1 receptors at the endoplasmic reticulum render cytotoxicity to physiologically relevant concentrations of dopamine in a nuclear factor-κB/Bcl-2-dependent mechanism: potential relevance to Parkinson's disease.The Journal of pharmacology and experimental therapeutics · 2012Article
- Oxidative stress in a model of toxic demyelination in rat brain: the effect of piracetam and vinpocetine.Neurochemical research · 2011Article
- Dopamine modifies oxygen consumption and mitochondrial membrane potential in striatal mitochondria.Molecular and cellular biochemistry · 2010Article
- Vulnerability of mesostriatal dopaminergic neurons in Parkinson's disease.Frontiers in neuroanatomy · 2010Article
- Targets for neuroprotection in Parkinson's disease.Biochimica et biophysica acta · 2009Review
- Intranigral dopamine toxicity and alpha-synuclein response in rats.Neurochemical research · 2006Article
- The generation of dopaminergic neurons by human neural stem cells is enhanced by Bcl-XL, both in vitro and in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Multicistronic lentiviral vector-mediated striatal gene transfer of aromatic L-amino acid decarboxylase, tyrosine hydroxylase, and GTP cyclohydrolase I induces sustained transgene expression, dopamine production, and functional improvement in a rat model of Parkinson's disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- The cell biology of alpha-synuclein: a sticky problem?Neuromolecular medicine · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease is a progressive neurological disease caused by rather selective degeneration of the dopaminergic neurons in the substantia nigra. Though subject to intensive research, the etiology of this nigral loss is still undetermined and treatment is basically symptomatic. The current major hypothesis is that nigral neuronal death in PD is due to excessive oxidative stress generated by auto and enzymatic oxidation of the endogenous neurotransmitter dopamine (DA), the formation of neuromelanin (NM) and the presence of a high concentration of iron. In this review article although we concisely describe the effects of NM and iron on neuronal survival, we mainly focus on the molecular mechanisms of DA-induced apoptosis. DA exerts its toxic effects through its oxidative metabolites either in vitro or in vivo The oxidative metabolites then activate a very intricate web of signals, which culminate in cell death. The signal transduction pathways and genes, which are associated with DA toxicity are described in detail.
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.