Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 May;42(5):416-425.
doi: 10.1007/s12272-019-01133-0. Epub 2019 Mar 4.

Significant roles of neuroinflammation in Parkinson's disease: therapeutic targets for PD prevention

Affiliations
Review

Significant roles of neuroinflammation in Parkinson's disease: therapeutic targets for PD prevention

Yujeong Lee et al. Arch Pharm Res. 2019 May.

Abstract

Glial cells outnumber neurons in the brain and play important roles in the neuroinflammation that accompanies brain damage in neurodegenerative diseases. In Parkinson's disease (PD), dopaminergic neuronal loss is accompanied by inflammatory changes in microglia, astrocytes, innate immune cells, and infiltrating peripheral immune cells. Neuroinflammation is probably a fundamental immune response to protect neurons from harm and compensate for neuronal damage, but at the same time, its neurotoxic effects exacerbate neuron damage. Furthermore, neuroinflammatory response is regulated by immune cells, such as microglia, astrocytes, and peripheral immune cells, and by cytokines and chemokines. Accordingly, it is crucial that we understand how such immune cells in the brain regulate neuroinflammatory responses in PD pathology. This review describes the roles played by glia-mediated neuroinflammation in PD, both good and bad, and the therapeutic strategies used to treat PD.

Keywords: A1 astrocyte; A2 astrocyte; Glia; Microglia; Neuroinflammation; Parkinson’s disease.

PubMed Disclaimer

Similar articles

Cited by

MeSH terms

Substances

LinkOut - more resources