ReviewJournal of molecular neuroscience : MN2004
Pathological proteins in Parkinson's disease: focus on the proteasome.
Review in Journal of molecular neuroscience : MN, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 60 citations in OpenAlex.
- Is There a Place for Lewy Bodies before and beyond Alpha-Synuclein Accumulation? Provocative Issues in Need of Solid Explanations.International journal of molecular sciences · 2024Review
- Multifunctional role of natural products for the treatment of Parkinson's disease: At a glance.Frontiers in pharmacology · 2022Review
- 27-Hydroxycholesterol increases α-synuclein protein levels through proteasomal inhibition in human dopaminergic neurons.BMC neuroscience · 2018Article
- Palmitic Acid-Enriched Diet Increases α-Synuclein and Tyrosine Hydroxylase Expression Levels in the Mouse Brain.Frontiers in neuroscience · 2018Article
- Detection of active proteasome structures in brain extracts: proteasome features of August rat brain with violations in monoamine metabolism.Oncotarget · 2017Article
- Catecholamine autotoxicity. Implications for pharmacology and therapeutics of Parkinson disease and related disorders.Pharmacology & therapeutics · 2014Review
- MPP+-induces PUMA- and p53-dependent, but ATF3-independent cell death.Toxicology letters · 2013Article
- Agrochemicals, α-synuclein, and Parkinson's disease.Molecular neurobiology · 2013Review
- Role of α-synuclein penetration into the membrane in the mechanisms of oligomer pore formation.The FEBS journal · 2012Article
- 6-OHDA generated ROS induces DNA damage and p53- and PUMA-dependent cell death.Molecular neurodegeneration · 2011Article
- Neuroprotection of pramipexole in UPS impairment induced animal model of Parkinson's disease.Neurochemical research · 2010Article
- Parkin reverses intracellular beta-amyloid accumulation and its negative effects on proteasome function.Journal of neuroscience research · 2010Article
- A critical evaluation of the ubiquitin-proteasome system in Parkinson's disease.Biochimica et biophysica acta · 2009Review
- Trends in the molecular pathogenesis and clinical therapeutics of common neurodegenerative disorders.International journal of molecular sciences · 2009Review
- Location, location, location: altered transcription factor trafficking in neurodegeneration.Journal of neuropathology and experimental neurology · 2007Review
- Lewy bodies.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) is a multifactorial disease that appears to arise from the effects of both genetic and environmental influences. Pesticides and heavy metals are the principle environmental factors that appear to impact on PD. The known genetic factors include multiple genes that have been identified in related parkinsonian syndromes, as well as alpha-synuclein. Genes associated with either PD or Parkinson-related disorders include parkin, DJ-1, ubiquitin C-terminal hydrolase isozyme L1 (UCH-L1), nuclear receptor-related factor 1, and alpha-synuclein. Alpha-synuclein is particularly notable because it aggregates readily and is the main component of Lewy bodies (LBs). Aggregated alpha-synuclein binds the proteasome and potently inhibits proteasomal activity. Because ubiquitin accumulates in LBs, and parkin and UCH-L1 also interact with the ubiquitin proteasomal system, proteasomal dysfunction is thought to contribute to the pathophysiology of PD. Increasing numbers of experiments suggest that neurotoxins might interact with alpha-synuclein or other Parkinson-related proteins to contribute to the pathophysiology of PD. Transgenic animal models overexpressing alpha-synuclein develop age-dependent motor dysfunction and inclusions in the brain stem that contain alpha-synuclein. These models are very helpful in elucidating the pathophysiology of PD but do not completely recapitulate the disease process. The relationship between these transgenic models and PD is a subject of intense investigation.
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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.