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Review
. 2020 Nov 10;21(22):8421.
doi: 10.3390/ijms21228421.

Neurodegeneration and Inflammation-An Interesting Interplay in Parkinson's Disease

Affiliations
Review

Neurodegeneration and Inflammation-An Interesting Interplay in Parkinson's Disease

Chrysoula Marogianni et al. Int J Mol Sci. .

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder, caused by, so far, unknown pathogenetic mechanisms. There is no doubt that pro-inflammatory immune-mediated mechanisms are pivotal to the pathogenicity and progression of the disease. In this review, we highlight the binary role of microglia activation in the pathophysiology of the disorder, both neuroprotective and neuromodulatory. We present how the expression of several cytokines implicated in dopaminergic neurons (DA) degeneration could be used as biomarkers for PD. Viral infections have been studied and correlated to the disease progression, usually operating as trigger factors for the inflammatory process. The gut-brain axis and the possible contribution of the peripheral bowel inflammation to neuronal death, mainly dopaminergic neurons, seems to be a main contributor of brain neuroinflammation. The role of the immune system has also been analyzed implicating a-synuclein in the activation of innate and adaptive immunity. We also discuss therapeutic approaches concerning PD and neuroinflammation, which have been studied in experimental and in vitro models and data stemming from epidemiological studies.

Keywords: Parkinson’s; autoimmunity; neurodegeneration; neuroinflammation.

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Conflict of interest statement

The authors declare no conflict of interest.

References

    1. Dorsey E., Constantinescu R., Thompson J.P., Biglan K.M., Holloway R.G., Kieburtz K., Marshall F.J., Ravina B.M., Schifitto G., Siderowf A., et al. Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030. Neurology. 2007;68:384–386. doi: 10.1212/01.wnl.0000247740.47667.03. - DOI - PubMed
    1. Tanner C.M., Goldman S.M. Epidemiology of Parkinson’s disease. Neurol. Clin. 1996;14:317–335. doi: 10.1016/S0733-8619(05)70259-0. - DOI - PMC - PubMed
    1. Liu B., Gao H.M., Hong J.S. Parkinson’s disease and exposure to infectious agents and pesticides and the occurrence of brain injury: Role of neuroinflammation. Environ. Health Perspect. 2003;111:1065–1073. doi: 10.1289/ehp.6361. - DOI - PMC - PubMed
    1. Boyko A.A., Troyanova N.I., Kovalenko E.I., Sapozhnikov A.M. Similarity and Differences in Inflammation-Related Characteristics of the Peripheral Immune System of Patients with Parkinson’s and Alzheimer’s Diseases. Int. J. Mol. Sci. 2017;18:2633. doi: 10.3390/ijms18122633. - DOI - PMC - PubMed
    1. Nandipati S., Litvan I. Environmental Exposures and Parkinson’s Disease. Int. J. Environ. Res. Public Health. 2016;13:881. doi: 10.3390/ijerph13090881. - DOI - PMC - PubMed

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