Cited by 5,469Parkinson's Disease Mechanisms and TreatmentsNuclear Receptors and SignalingDeep Brain Stimulation and Movement Disorders

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Parkinson's Disease

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Dauer, William, Przedborski, Serge·2003·Neuron

DOI 10.1016/s0896-6273(03)00568-3

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Abstract

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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Authors: Dauer, W., & Przedborski, S.
Affiliations: Columbia University (US)
Corresponding author: Przedborski, Serge
ORCID: Dauer, William
Przedborski, Serge
Venue: Neuron
Publisher: Elsevier BV
Published: 2003-09
Volume: 39
Issue: 6
Pages: 889-909
ISSN: 0896-6273 (ISSN-L)
DOI: 10.1016/s0896-6273(03)00568-3
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: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 3607 d)
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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