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
. 2021 Nov 26;11(12):1774.
doi: 10.3390/biom11121774.

Microglial Potassium Channels: From Homeostasis to Neurodegeneration

Germana Cocozza  1 , Stefano Garofalo  2 , Riccardo Capitani  2 , Giuseppina D'Alessandro  1   2 , Cristina Limatola  1   3
Affiliations
Review

Microglial Potassium Channels: From Homeostasis to Neurodegeneration

Germana Cocozza et al. Biomolecules. .

Abstract

The growing interest in the role of microglia in the progression of many neurodegenerative diseases is developing in an ever-expedited manner, in part thanks to emergent new tools for studying the morphological and functional features of the CNS. The discovery of specific biomarkers of the microglia phenotype could find application in a wide range of human diseases, and creates opportunities for the discovery and development of tailored therapeutic interventions. Among these, recent studies highlight the pivotal role of the potassium channels in regulating microglial functions in physiological and pathological conditions such as Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis. In this review, we summarize the current knowledge of the involvement of the microglial potassium channels in several neurodegenerative diseases and their role as modulators of microglial homeostasis and dysfunction in CNS disorders.

Keywords: CNS; microglia; neurodegenerative disease; neuroinflammation; potassium channel.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic illustration describing the role of microglial K+ channels in NDD. Microglial cells increase the expression/activity of Kv1.3 and KCa3.1 in several neurodegenerative diseases, losing their homeostatic functions. This is associated with the release of inflammatory cytokines such as IFN-γ and TNF-α, production of noxious substances (ROS), reduced phagocytic activity, which are involved in inflammation-mediated neurotoxicity. Created in BioRender.com.
See this image and copyright information in PMC

References

    1. Feigin V.L., Nichols E., Alam T., Bannick M.S., Beghi E., Blake N., Culpepper W.J., Dorsey E.R., Elbaz A., Ellenbogen R.G., et al. Global, regional, and national burden of neurological disorders, 1990–2016: A systematic analysis for the global burden of disease study 2016. Lancet Neurol. 2019;18:459–480. doi: 10.1016/S1474-4422(18)30499-X. - DOI - PMC - PubMed
    1. Perry V.H., Teeling J. Microglia and macrophages of the central nervous system: The contribution of microglia priming and systemic inflammation to chronic neurodegeneration. Sem. Immunopathol. 2013;35:601–612. doi: 10.1007/s00281-013-0382-8. - DOI - PMC - PubMed
    1. Schwartz M., Kipnis J., Rivest S., Prat A. How do immune cells support and shape the brain in health, disease, and aging? J. Neurosci. 2013;33:17587–17596. doi: 10.1523/JNEUROSCI.3241-13.2013. - DOI - PMC - PubMed
    1. Nimmerjahn A., Kirchhoff F., Helmchen F. Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo. Science. 2005;308:1314–1318. doi: 10.1126/science.1110647. - DOI - PubMed
    1. Butovsky O., Jedrychowski M.P., Moore C.S., Cialic R., Lanser A.J., Gabriely G., Koeglsperger T., Dake B., Wu P.M., Doykan C.E., et al. Identifcation of a unique TGF-β-dependent molecular and functional signature in microglia. Nat. Neurosci. 2014;17:131–143. doi: 10.1038/nn.3599. - DOI - PMC - PubMed

Publication types