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Cited by 586

Neuroinflammation in Parkinson's disease

Hirsch, Etienne C., Vyas, Sheela, Hunot, Stéphane·2012·Parkinsonism & Related Disorders
DOI 10.1016/s1353-8020(11)70065-7
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Abstract

Both epidemiological and genetic studies support a role of neuroinflammation in the pathophysiology of Parkinson's disease (PD). Furthermore, post mortem studies confirm the involvement of innate as well as adaptive immunity in the affected brain regions in patients with PD. Indeed, activated microglial cells and T lymphocytes have been detected in the substantia nigra of patients concomitantly with an increased expression of pro-inflammatory mediators. Preclinical investigations conducted in various animal models of PD indicate that inflammatory processes are instrumental in neuronal cell death even though they are unlikely to be a primary cause for neuronal loss. Neuroinflammatory processes in PD are rather involved in self-perpetuating deleterious events that lead to protracted neuronal degeneration. In line with this, recent data indicate that glucocorticoid receptors are important in curtailing microglial reactivity, and deregulation in their activity in PD could lead to sustained inflammation-mediated degeneration. Altogether, neuroinflammatory processes might represent a target for neuroprotection in PD.

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  • Dysregulation of microglia functions contributes to the pathogenesis of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and Huntington's disease.

    “Dysregulation of microglia functions contribute to the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD) (6–8), Parkinson’s disease (PD) (9–12) and Huntington’s disease (HD) (13–15).”

    From An environment-dependent transcriptional network specifies human microglia identity (2017) · cites this paper as [9]

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Authors
Hirsch, E. C., Vyas, S., & Hunot, S.
Venue
Parkinsonism & Related Disorders
Publisher
Elsevier BV
Published
2012-01
Volume
18
Pages
S210-S212
ISSN
1353-8020
DOI
10.1016/s1353-8020(11)70065-7
Cited by
586
References
3
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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