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Vulnerability of mesostriatal dopaminergic neurons in Parkinson’s disease
Open accessAbstract
The term vulnerability was first associated with the midbrain dopaminergic neurons 85 years ago, before they were identified as monoaminergic neurons, when Foix and Nicolesco (1925) reported the loss of neuromelanin containing neurons in the midbrain of patients with post-encephalitic Parkinson's disease (PD). A few years later, Hassler (1938) showed that degeneration is more intense in the ventral tier of the substantia nigra compacta than in its dorsal tier and the ventral tegmental area (VTA), outlining the concept of differential vulnerability of midbrain dopaminergic (DA-) neurons. Nowadays, we know that other neuronal groups degenerate in PD, but the massive loss of nigral DA-cells is its pathological hallmark, having a pivotal position in the pathophysiology of the disease as it is responsible for the motor symptoms. Data from humans as well as cellular and animal models indicate that DA-cell degeneration is a complex process, probably precipitated by the convergence of different risk factors, mediated by oxidative stress, and involving pathogenic factors arising within the DA-neuron (intrinsic factors), and from its environment and distant interconnected brain regions (extrinsic factors). In light of current data, intrinsic factors seem to be preferentially involved in the first steps of the degenerative process, and extrinsic factors in its progression. A controversial issue is the relative weight of the impairment of common cell functions, such as energy metabolism and proteostasis, and specific dopaminergic functions, such as pacemaking activity and DA handling, in the pathogenesis of DA-cell degeneration. Here we will review the current knowledge about the relevance of these factors at the beginning and during the progression of PD, and in the differential vulnerability of midbrain DA-cells.
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“Although dopaminergic neurons throughout the midbrain degenerate during Parkinson’s disease, death of SNc dopamine neurons is more pronounced (Gonzalez-Hernandez et al., 2010).”
From Local cues establish and maintain region-specific phenotypes of basal ganglia microglia (2017) · cites this paper as Gonzalez-Hernandez et al., 2010
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BackgroundLocal cues establish and maintain region-specific phenotypes of basal ganglia microglia
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“…mishandling, impairment of the ubiquitin–proteasome pathway and inflammation contribute to SN DA degeneration and sporadic as well as familial PD (Gonzalez-Hernandez et al. 2010; Guzman et al. 2010; Obeso and Lanciego 2011; Coskun et al. 2012; Sulzer and Surmeier 2013; Beilina and Cookson 2015;…”
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“However, the mechanisms responsible for this difference have not been clarified [4].”
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“…known that phenotypic specificities determine how individuals react to drugs (Batist et al., 2011; Callahan and Abercrombie, 2011), to infections (González-Hernández et al., 2010), or how predisposed they are to inherited diseases such as cystic fibrosis (Gu et al., 2009; Antigny et al., 2011),…”
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“Clinical analysis on postmortem of brain sample of patients with PD indicates extensive damage of the midbrain dopaminergic neurons.(4) The presence of >-synuclein in LB reveals its central role in pathogenesis of PD.”
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“Regarding their implication in PD, there is a well-documented and abundant literature investigating the factors involved in the vulnerability and degeneration of SNc DA neurons (Olanow and Tatton, 1999; González-Hernández, 2010; Surmeier et al., 2010; Dragicevic et al., 2015).”
BackgroundSHH mediated human dopaminergic neuron differentiation is facilitated by transcription factor ZIC3
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Metadata
- Authors
- González-Hernández, T.
- Venue
- Frontiers in Neuroanatomy
- Publisher
- Frontiers Media SA
- Published
- 2010
- Volume
- 4
- Pages
- 140-140
- ISSN
- 1662-5129 (ISSN-L)
- PMC
- PMC2978035
- OpenAlex
- W2123571361
- Cited by
- 65
- References
- 263
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 4 · 2019: 5 · 2018: 2 · 2017: 10 · 2016: 6 · 2015: 3 · 2014: 7 · 2013: 2 · 2012: 11
- FWCI
- 3.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Neuroanatomy (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Fundación Canaria de Investigación y Salud
- Department of Science and Technology, Ministry of Science and Technology, India
- Ministerio de Ciencia e Innovación
- Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas
- Instituto de Salud Carlos III
- 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, substantia nigra pars compacta, ventral tegmental area, oxidative stress, intrinsic and extrinsic risk factors, energy metabolism, proteostasis
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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