Surveillance, phagocytosis, and inflammation: how never-resting microglia influence adult hippocampal neurogenesis

Amanda Sierra1, Sol Beccari2, Irune Diaz-Aparicio2

  • 1Ikerbasque Foundation, 48011 Bilbao, Spain ; Achucarro Basque Center for Neuroscience, Bizkaia Science and Technology Park, 48170 Zamudio, Spain ; Department of Neurosciences, University of the Basque Country, 48940 Leioa, Spain.

Neural Plasticity
|April 29, 2014
PubMed

Insights

Microglia cells, traditionally linked to brain inflammation, also play a positive role in healthy brain functions. This review explores their impact on neurogenesis, learning, and memory, especially during stress and aging.

Area of Science:

  • Neuroscience
  • Immunology
  • Cellular Biology

Background:

  • Microglia are key regulators of brain inflammation, traditionally studied in disease contexts.
  • Recent findings highlight microglia's crucial roles in normal brain function and cellular plasticity.
  • Surveillant microglia are increasingly recognized as effectors in the healthy brain.

Purpose of the Study:

  • To review the multifaceted roles of microglia in adult hippocampal neurogenesis.
  • To examine how inflammation affects microglia during chronic stress, aging, and neurodegenerative diseases.
  • To emphasize the molecular mechanisms and functional consequences of microglial activity on learning and memory.

Main Methods:

  • Literature review of studies on microglia, neurogenesis, and inflammation.
  • Analysis of molecular mechanisms underlying microglial regulation.
  • Synthesis of findings on functional outcomes for cognition.

Main Results:

  • Microglia contribute to adult hippocampal neurogenesis.
  • Inflammation significantly modulates microglial functions in aging and disease.
  • Microglial activity impacts learning and memory through various molecular pathways.

Conclusions:

  • Microglia are essential for maintaining brain health and plasticity, not just in disease.
  • Understanding microglial regulation by inflammation is critical for cognitive function.
  • Targeting microglial pathways may offer therapeutic strategies for cognitive decline.

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