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Microglial plasticity across development mediates infantile amnesia.

Erika Stewart1,2, Louisa G Zielke1,2, Gabrielle Guillaume1,2

  • 1School of Biochemistry and Immunology, Trinity College Dublin, Dublin, Ireland.

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|November 24, 2025
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Summary
This summary is machine-generated.

Microglia, immune cells in the brain, regulate early childhood memory. Inhibiting microglial activity in infancy prevents infantile amnesia, revealing their role in memory persistence.

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Immunology

Background:

  • Infantile amnesia is the inability to recall early childhood memories.
  • The mechanisms behind infantile amnesia are not well understood.
  • Microglia, the brain's immune cells, influence brain development and memory.

Purpose of the Study:

  • To understand the mechanistic basis of infantile amnesia.
  • To investigate the role of microglia in memory formation and retrieval during infancy.

Main Methods:

  • Profiling microglial morphology during the postnatal period.
  • Pharmacological inhibition of microglial activity in infant rodents.
  • Activity-dependent tagging of infant-encoded memory traces (engrams).
  • Analyzing microglia-engram cell interactions in the amygdala.

Main Results:

  • Microglial activity changes correlate with the onset of infantile forgetting.
  • Inhibiting microglia during a critical window prevented infantile amnesia for contextual fear memories.
  • Microglial inhibition affected engram size, reactivation, and microglia-engram cell interactions.
  • Microglial dysfunction in maternal immune activation models was linked to a lack of infantile amnesia.

Conclusions:

  • Microglia are key regulators of memory accessibility and persistence in infancy.
  • Microglial activity actively modulates infant memory.
  • Dysfunctional microglia may contribute to memory impairments in neurodevelopmental disorders.