Nitric oxide synthase and neuronal vulnerability in parkinson's disease
Abstract
Parkinson's disease is characterized by a loss of dopaminergic neurons in the mesencephalon. Although the mechanism of this neuronal loss is still unknown, oxidative stress is very likely involved in the cascade of events leading to nerve cell death. Since nitric oxide could be involved in the production of free radicals, we analysed, using immunohistochemistry and histochemistry, the production systems of nitric oxide in the mesencephalon of four patients with idiopathic Parkinson's disease and three matched control subjects. Using specific antibodies directed against the inducible isoform of nitric oxide synthase (the enzyme involved in the synthesis of nitric oxide), we found evidence to suggest that this isoform was present solely in glial cells displaying the morphological characteristics of activated macrophages. Immunohistochemical analysis performed with antibodies against the neuronal isoform of nitric oxide synthase, however, revealed perikarya and processes of neurons but no glial cell staining. The number of nitric oxide synthase-containing cells was investigated by histoenzymology, using the NADPH-diaphorase activity of nitric oxide synthase. Histochemistry revealed (i) a significant increase in NADPH-diaphorase-positive glial cell density in the dopaminergic cell groups characterized by neuronal loss in Parkinson's disease and (ii) a neuronal loss in Parkinson's disease that was two-fold greater for pigmented NADPH-diaphorase-negative neurons than for pigmented NADPH-diaphorase-positive neurons. These data suggest a potentially deleterious role of glial cells producing excessive levels of nitric oxide in Parkinson's disease, which may be neurotoxic for a subpopulation of dopaminergic neurons, especially those not expressing NADPH-diaphorase activity. However, it cannot be excluded that the presence of glial cells expressing nitric oxide synthase in the substantia nigra of patients with Parkinson's disease represents a consequence of dopaminergic neuronal loss.
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Analysis of post-mortem human brain samples revealed increased levels of iNOS in PD.
“Analysis of post-mortem human brain samples revealed increased levels of iNOS PD.460”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [460]
Microglial activation markers such as iNOS, COX, and CD68 are upregulated in PD patients.
“Other microglial activation markers, such as pro-inflammatory enzymes like iNOS and COX211,212 and phagocytosis-associated marker CD68,213 were also upregulated in PD patients.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [211]
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- Authors
- Hunot, S., Boissière, F., Faucheux, B., Brugg, B., Mouatt-Prigent, A., Agid, Y., & Hirsch, E. C.
- Affiliations
- Inserm (FR)
- ORCID
- Hunot, S.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 1996-05
- Volume
- 72
- Issue
- 2
- Pages
- 355-363
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2006497054
- Cited by
- 595
- References
- 58
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 6 · 2023: 14 · 2022: 23 · 2021: 16 · 2020: 12 · 2019: 13 · 2018: 18 · 2017: 17 · 2016: 26 · 2015: 24 · 2014: 32 · 2013: 25 · 2012: 32
- FWCI
- 11.15
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, nitric oxide synthase, inducible nitric oxide synthase, neuronal vulnerability, dopaminergic neuron loss, substantia nigra, glial cells, macrophage activation, NADPH-diaphorase, oxidative stress, neurotoxicity, free radicals
- MeSH terms
- Aged, Aged, 80 and over, Animals, Female, Humans, Image Processing, Computer-Assisted, Immunohistochemistry, Male, Mesencephalon, Mice, Inbred C57BL, Middle Aged, NADPH Dehydrogenase, Neurons, Parkinson Disease, Macrophages, Peritoneal, Nitric Oxide Synthase, Mice, In Vitro Techniques
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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