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Mini Review ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Cell. Neurosci. | doi: 10.3389/fncel.2019.00522

The Rules of Engagement: Do microglia seal the fate in the inverse relation of glioma and Alzheimer’s disease?

  • 1Toxicology Unit, Institute of Environmental Medicine, Sweden
  • 2Karolinska Institutet (KI), Sweden
  • 3Neuroscience Center, University of Helsinki, Finland

Microglia, the immune cells of the brain, play a major role in the maintenance of brain homeostasis and constantly screen the brain environment to detect any infection or damage. Once activated by a stimulus, microglial cells initiate an immune response followed by the resolution of brain inflammation. A failure or deviation in the housekeeping function of these guardian cells can lead to multiple diseases, including brain cancer and neurodegenerative diseases such as Alzheimer’s disease (AD). A small number of studies have investigated the causal relation of both diseases, thereby revealing an inverse relationship where cancer patients have a reduced risk to develop AD and vice versa. In this review we aim to shed light on the role of microglia in the fate to develop specifically glioma as one type of cancer or AD. We will examine the common and/or opposing genetic predisposition as well as associated pathways of these diseases to unravel a possible involvement of microglia in the occurrence of either disease. Lastly, a set of guidelines will be proposed for future research and diagnostics to clarify and improve the knowledge on the role of microglia in the decision towards one pathology or another.

Keywords: Disease-associated microglia, Glioma, Alzheimer's disease, Inverse correlation, Risk Genes

Received: 02 Oct 2019; Accepted: 07 Nov 2019.

Copyright: © 2019 Cheray, Stratoulias, Joseph and Grabert. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Prof. Bertrand Joseph, Karolinska Institutet (KI), Solna, 171 77, Stockholm, Sweden,
Dr. Kathleen Grabert, Karolinska Institutet (KI), Solna, 171 77, Stockholm, Sweden,