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Related Experiment Video

Updated: Jan 20, 2026

Electrophysiological Measurement of Noxious-evoked Brain Activity in Neonates Using a Flat-tip Probe Coupled to Electroencephalography
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Late Brain Involvement after Neonatal Immune Activation.

Paula Dias1, Viviane Freiberger1, Letícia Ventura1

  • 1Research Group on Neurodevelopment of Childhood and Adolescence, Laboratory of Experimental Neuroscience, Postgraduate Program in Health Sciences, University of South Santa Catarina, Palhoça, SC, Brazil.

Biomed Research International
|August 31, 2019
PubMed
Summary

Neonatal immune activation, triggered by lipopolysaccharide (LPS), leads to long-term visuospatial memory deficits and neuroinflammation in mice. This early-life immune challenge is linked to increased GSK-3β and Tau protein expression, suggesting a potential pathway to neurodegeneration.

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Area of Science:

  • Neuroscience
  • Immunology
  • Developmental Biology

Background:

  • The immature neonatal immune system is vulnerable to infections, and immune activation can compromise the blood-brain barrier.
  • Neonatal immune activation may trigger central nervous system (CNS) inflammation, affecting behavior and neurochemistry.
  • Neuroinflammation is hypothesized to play a role in neurodegenerative diseases like Alzheimer's disease (AD).

Purpose of the Study:

  • To investigate the long-term effects of neonatal immune activation on visuospatial memory.
  • To assess neuroinflammation by measuring cytokine levels in the hippocampus and cortex.
  • To evaluate the expression of tau and GSK-3β proteins in the brain following neonatal endotoxemia.

Main Methods:

  • C57BL/6 mice at two days of age received a single lipopolysaccharide (LPS) injection to induce neonatal endotoxemia.
  • Visuospatial memory was assessed at 60, 120, and 180 days of age.
  • Hippocampus and cortex tissues were analyzed for cytokine levels (TNF-α, IL-1β) and protein expression (GSK-3β, Tau).

Main Results:

  • Neonatal LPS exposure resulted in visuospatial memory impairment at 120 and 180 days of age.
  • Elevated TNF-α and IL-1β levels were observed in the hippocampus and cortex at 60 days.
  • Increased GSK-3β expression was noted in the hippocampus (60, 120, 180 days) and cortex (120, 180 days).
  • Tau protein expression was elevated in the hippocampus and cortex at 120 days, and in the hippocampus at 180 days.

Conclusions:

  • Neonatal immune activation is associated with lasting visuospatial memory deficits.
  • Early-life immune challenges can induce persistent neuroinflammation and alter key protein expressions (GSK-3β, Tau).
  • These findings suggest a potential link between neonatal immune activation and long-term neurodegenerative processes.