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PERSPECTIVE article

Front. Mol. Neurosci.
Sec. Molecular Signalling and Pathways
Volume 17 - 2024 | doi: 10.3389/fnmol.2024.1441691
This article is part of the Research Topic Neuro-Immune Interplay: Unraveling the Complexities of Neurological Complications and Immunology View all articles

Common Cytokine Receptor Gamma Chain Family Cytokines Activate MAPK, PI3K, and JAK/STAT Pathways in Microglia to Influence Alzheimer's Disease

Provisionally accepted
Hannah Zuppe Hannah Zuppe 1Erin G. Reed Erin G. Reed 2*
  • 1 Kent State University, Kent, Ohio, United States
  • 2 Northeast Ohio Medical University, Rootstown, United States

The final, formatted version of the article will be published soon.

    Dementia is an umbrella term used to describe deterioration of cognitive function. It is the seventh leading cause of death and is one of the major causes of dependence among older people globally. Alzheimer's Disease (AD) contributes to approximately 60-70% of dementia cases and is characterized by the accumulation of amyloid plaques and tau tangles in the brain.Neuroinflammation is now widely accepted as another disease hallmark, playing a role in both the response to and the perpetuation of disease processes. Microglia are brain-resident immune cells that are initially effective at clearing amyloid plaques but contribute to the damaging inflammatory milieu of the brain as disease progresses. Circulating peripheral immune cells contribute to this inflammatory environment through cytokine secretion, creating a positive feedback loop with the microglia. One group of these peripherally derived cytokines acting on microglia is the common cytokine receptor γ chain family. These cytokines bind heterodimer receptors to activate three major signaling pathways: MAPK, PI3K, and JAK/STAT. This perspective will look at the mechanisms of these three pathways in microglia and highlight the future directions of this research and potential therapeutics.

    Keywords: Alzheimer's disease, Neuroinflammation, Microglia, Interleukins, cellular signaling

    Received: 31 May 2024; Accepted: 30 Aug 2024.

    Copyright: © 2024 Zuppe and Reed. 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) or licensor 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: Erin G. Reed, Northeast Ohio Medical University, Rootstown, United States

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