ArticleNeuroscience letters2006
Parkin is protective for substantia nigra dopamine neurons in a tau gene transfer neurodegeneration model.
Article in Neuroscience letters, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 50 citations in OpenAlex.
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Exploration of Aberrant E3 Ligases Implicated in Alzheimer's Disease and Development of Chemical Tools to Modulate Their Function.Frontiers in cellular neuroscience · 2021Review
- PINK1/PARKIN signalling in neurodegeneration and neuroinflammation.Acta neuropathologica communications · 2020Review
- Mitochondrial E3 Ubiquitin Ligase Parkin: Relationships with Other Causal Proteins in Familial Parkinson's Disease and Its Substrate-Involved Mouse Experimental Models.International journal of molecular sciences · 2020Review
- Induced pluripotent stem cell-based modeling of mutant LRRK2-associated Parkinson's disease.The European journal of neuroscience · 2019Review
- Twenty years since the discovery of the parkin gene.Journal of neural transmission (Vienna, Austria : 1996) · 2017Review
- Recent advances in methamphetamine neurotoxicity mechanisms and its molecular pathophysiology.Behavioural neurology · 2015Review
- Overexpression of parkin in the rat nigrostriatal dopamine system protects against methamphetamine neurotoxicity.Experimental neurology · 2013Article
- RETRACTED: Wild type and P301L mutant Tau promote neuro-inflammation and α-Synuclein accumulation in lentiviral gene delivery models.Molecular and cellular neurosciences · 2012Article
- Inflammation in the early stages of neurodegenerative pathology.Journal of neuroimmunology · 2011Review
- The Relationship between Parkin and Protein Aggregation in Neurodegenerative Diseases.Frontiers in psychiatry · 2010Article
- Versatile somatic gene transfer for modeling neurodegenerative diseases.Neurotoxicity research · 2009Review
- Mimicking aspects of frontotemporal lobar degeneration and Lou Gehrig's disease in rats via TDP-43 overexpression.Molecular therapy : the journal of the American Society of Gene Therapy · 2009Article
- Parkin attenuates wild-type tau modification in the presence of beta-amyloid and alpha-synuclein.Journal of molecular neuroscience : MN · 2009Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Parkin is a ubiquitin ligase involved in the ubiquitin-proteasome system. Elevating parkin expression in cells reduces markers of oxidative stress while blocking parkin expression increases oxidative stress. In parkin gene knock down mouse and fly models, mitochondria function is deficient. Parkin is neuroprotective against a variety of toxic insults, while it remains unclear which of the above properties of parkin may mediate the protective actions. One of the models for which parkin is protective is overexpression of alpha-synuclein, a protein that self-aggregates in Parkinson disease. The microtubule-associated protein tau is another protein that self-aggregates in specific neurodegenerative diseases that also involve loss of dopamine neurons such as frontotemporal dementia with parkinsonism linked to chromosome 17, progressive supranuclear palsy and corticobasal degeneration. We recently developed a tau-induced dopaminergic degeneration model in rats using adeno-associated virus vectors. In this study, we successfully targeted either a mixed tau/parkin vector or mixed tau/control vector to the rat substantia nigra. While there was significant loss of dopamine neurons in the tau/control group relative to uninjected substantia nigra, there was no cell loss in the tau/parkin group. We found no difference in total tau levels between tau/control and tau/parkin groups. Parkin therefore protects dopamine neurons against tau as it does against alpha-synuclein, which further supports parkin as a therapeutic target for diseases involving loss of dopamine neurons.
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.