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Related Experiment Video

Updated: Mar 15, 2026

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

Microglia Priming with Aging and Stress.

Anzela Niraula^1,2, John F Sheridan^2,3, Jonathan P Godbout^1,2,4

¹Department of Neuroscience, The Ohio State University, Columbus, OH, USA.

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology

|September 9, 2016

Summary

This summary is machine-generated.

As the global population ages, brain inflammation and microglial sensitization worsen cognitive decline. Interventions like caloric restriction can reverse these aging-related deficits.

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Published on: October 27, 2019

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Last Updated: Mar 15, 2026

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

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Published on: January 30, 2014

Culturing Microglia from the Neonatal and Adult Central Nervous System

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Published on: August 9, 2013

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

Published on: October 27, 2019

Area of Science:

Neuroscience
Immunology
Gerontology

Background:

Global aging population presents significant health and socio-economic challenges.
Aging brains exhibit reduced neurogenesis, synaptic issues, metabolic stress, and inflammation.
These changes in rodent models correlate with cognitive decline and neurobehavioral deficits.

Purpose of the Study:

To review neuroinflammatory signaling and microglial sensitization in aging.
To explore the implications of psychological stress on aging-related neuroinflammation.
To discuss interventions that can reverse age-associated cognitive deficits.

Main Methods:

Review of clinical and experimental studies on aging and neuroinflammation.
Focus on the role of microglia in the aged brain.
Analysis of the impact of psychological stress on microglial function.

Main Results:

Aged microglia show dystrophic morphology, increased inflammatory markers, and decreased neuroprotection.
Aged microglia exhibit a 'primed' phenotype, increasing vulnerability to secondary insults.
Psychological stress can induce aging-like microglial sensitization.

Conclusions:

Microglial sensitization is a key feature of brain aging, exacerbating vulnerability.
Understanding neuroinflammation in aging is crucial for developing effective interventions.
Reversal of behavioral effects of aging is possible through interventions like caloric restriction.