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Related Experiment Video

Updated: May 25, 2026

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

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Published on: October 6, 2017

Neuroinflammation and synaptic loss.

Jagadeesh S Rao1, Matthew Kellom, Hyung-Wook Kim

  • 1Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg. 9, Rm. 1S126 MSC 0947, Bethesda, MD 20892-0947, USA. jrao@grc.nia.nih.gov

Neurochemical Research
|February 8, 2012
PubMed
Summary

Neuroinflammation, driven by activated glial cells releasing inflammatory signals, damages neurons by altering synaptic proteins. This synaptic damage is linked to cognitive decline in various brain diseases.

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An Engulfment Assay: A Protocol to Assess Interactions Between CNS Phagocytes and Neurons
07:38

An Engulfment Assay: A Protocol to Assess Interactions Between CNS Phagocytes and Neurons

Published on: June 8, 2014

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Neuroinflammation is a key factor in neurodegenerative, neuropsychiatric, and viral diseases.
  • Activated microglia and astrocytes release inflammatory mediators like cytokines and nitric oxide, activating signaling pathways.
  • Key cytokines, interleukin-1 beta and tumor necrosis factor alpha, influence gene transcription in the brain.

Purpose of the Study:

  • To explore the role of neuroinflammation in altering synaptic proteins.
  • To understand the impact of inflammatory processes on neuronal function and cognitive health.
  • To investigate the link between neuroinflammation, synaptic changes, and disease progression.

Main Methods:

  • Analysis of inflammatory mediator release (cytokines, chemokines, nitric oxide) from activated glial cells.
  • Investigation of signal transduction pathways activated during neuroinflammation.
  • Assessment of changes in synaptic protein expression (e.g., synaptophysin, drebrin) in response to inflammatory insults.

Main Results:

  • Neuroinflammation leads to the formation of pro-inflammatory products, including those from the arachidonic acid cascade.
  • Pro-inflammatory agents and cytotoxic products detrimentally affect neurons by altering synaptic proteins.
  • Both neuroinflammation and excitotoxic insults reduce critical synaptic markers like synaptophysin and drebrin.

Conclusions:

  • Synaptic protein loss, including pre- and post-synaptic components, accompanies neurodegenerative, neuropsychiatric illnesses, and viral infections.
  • These synaptic alterations are implicated in the progressive cognitive decline and behavioral changes observed in these conditions.
  • Targeting neuroinflammation may offer therapeutic strategies for preserving synaptic integrity and mitigating cognitive deficits.