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MINI REVIEW article

Front. Cell. Neurosci.
Sec. Non-Neuronal Cells
Volume 18 - 2024 | doi: 10.3389/fncel.2024.1456253
This article is part of the Research Topic 15 Years of Frontiers in Cellular Neuroscience: Microglia Origin and Phenotype Diversity View all articles

The intricate interplay between microglia and adult neurogenesis in Alzheimer's disease

Provisionally accepted
Melanie Meyer-Luehmann Melanie Meyer-Luehmann *Iris Früholz Iris Früholz
  • Neurology/Neurodegeneration, University of Freiburg, Freiburg, Germany

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

    Microglia, the resident immune cells of the central nervous system, play a crucial role in regulating adult neurogenesis and contribute significantly to the pathogenesis of Alzheimer's disease (AD). Under physiological conditions, microglia support and modulate neurogenesis through the secretion of neurotrophic factors, phagocytosis of apoptotic cells, and synaptic pruning, thereby promoting the proliferation, differentiation, and survival of neural progenitor cells (NPCs). However, in AD, microglial function becomes dysregulated, leading to chronic neuroinflammation and impaired neurogenesis. This review explores the intricate interplay between microglia and adult neurogenesis in health and AD, synthesizing recent findings to provide a comprehensive overview of the current understanding of microglia-mediated regulation of adult neurogenesis. Furthermore, it highlights the potential of microglia-targeted therapies to modulate neurogenesis and offers insights into potential avenues for developing novel therapeutic interventions.

    Keywords: Alzheimer's disease, amyloid plaques, Microglia, adult neurogenesis, neurodegeneration

    Received: 28 Jun 2024; Accepted: 26 Aug 2024.

    Copyright: © 2024 Meyer-Luehmann and Früholz. 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: Melanie Meyer-Luehmann, Neurology/Neurodegeneration, University of Freiburg, Freiburg, 79106, Germany

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.