The DOI matches its Crossref record; 243 of the 243 references it cites were found in a registry or an index.
Parkinson's Disease
Open accessAbstract
Parkinson's disease (PD) results primarily from the death of dopaminergic neurons in the substantia nigra. Current PD medications treat symptoms; none halt or retard dopaminergic neuron degeneration. The main obstacle to developing neuroprotective therapies is a limited understanding of the key molecular events that provoke neurodegeneration. The discovery of PD genes has led to the hypothesis that misfolding of proteins and dysfunction of the ubiquitin-proteasome pathway are pivotal to PD pathogenesis. Previously implicated culprits in PD neurodegeneration, mitochondrial dysfunction and oxidative stress, may also act in part by causing the accumulation of misfolded proteins, in addition to producing other deleterious events in dopaminergic neurons. Neurotoxin-based models (particularly MPTP) have been important in elucidating the molecular cascade of cell death in dopaminergic neurons. PD models based on the manipulation of PD genes should prove valuable in elucidating important aspects of the disease, such as selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process.
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In the citing paper
“The diagnosis of PD is reliant on clinical motor symptoms and neuroimaging; however, by the onset of symptoms, it is estimated that 50–70% of substantia nigra pars compacta dopaminergic neurons have already been lost [247, 248].”
From Extracellular vesicles as nanotheranostic platforms for targeted neurological disorder interventions (2024) · cites this paper as [248]
In the citing paper
“Neurotoxicants, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), paraquat, rotenone and 6-hydroxydopamine (6-OHDA), are commonly used to induce experimental PD models by disrupting mitochondria and increasing oxidative stress [9]”
From Healthy Human Fecal Microbiota Transplantation into Mice Attenuates MPTP-Induced Neurotoxicity via AMPK/SOD2 Pathway (2023) · cites this paper as [9]
In the citing paper
“PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the nerve terminals in the striatum (Dauer and Przedborski, 2003).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Dauer and Przedborski, 2003
In the citing paper
“Genetic factors include mutations in α-syn (Olanow and Tatton, 1999; Pérez and Arancibia, 2007), while mitochondrial dysfunction and oxidative stress may also act by causing the accumulation of misfolded proteins (Dauer and Przedborski, 2003).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Dauer and Przedborski, 2003
In the citing paper
“Mitochondrial dysfunction is implicated in the pathophysiology of Parkinson′s disease (PD), a common age-associated neurodegenerative disease characterized by intraneuronal inclusions (Lewy bodies) and progressive degeneration of the nigrostriatal dopamine (DA) system.”
From Progressive parkinsonism in mice with respiratory-chain-deficient dopamine neurons (2007) · cites this paper as [2]
In the citing paper
“In addition to mtDNA mutations, pathogenic mutations in several genes including α–synuclein, parkin, UCHL-1, DJ-1, PINK-1, LRRK-2, NURR-1, tau, and HtrA2 also directly or indirectly implicate a role of mitochondrial dysfunction in familial PD pathogenesis3, 28, 29.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [29]
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Self-citation
Metadata
- Authors
- Dauer, W., & Przedborski, S.
- Affiliations
- Columbia University (US)
- Corresponding author
- Przedborski, Serge
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2003-09
- Volume
- 39
- Issue
- 6
- Pages
- 889-909
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W62603772
- Cited by
- 5,469
- References
- 243
- Citations by year
- 2026: 167 · 2025: 250 · 2024: 287 · 2023: 288 · 2022: 309 · 2021: 301 · 2020: 312 · 2019: 294 · 2018: 328 · 2017: 329 · 2016: 276 · 2015: 267 · 2014: 273 · 2013: 268 · 2012: 229
- FWCI
- 13.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS 38586, R01NS042269, R01NS038586, NS11766-27A1, P50NS038370, NS 42269, NS38370)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Health Sciences › Medicine › Clinical Neurology › Deep Brain Stimulation and Movement Disorders
- Keywords
- Parkinson's disease, dopaminergic neuron loss, substantia nigra, neurodegeneration, protein misfolding, ubiquitin-proteasome system, mitochondrial dysfunction, oxidative stress, MPTP-induced neurotoxicity, neuroprotective therapy, disease models
- MeSH terms
- Animals, Disease Models, Animal, Humans, Neurons, Parkinson Disease
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