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Related Experiment Video

Updated: Jun 12, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Age-related neuroinflammatory changes negatively impact on neuronal function.

Marina A Lynch¹

¹Trinity College Institute of Neuroscience, Trinity College Dublin, Ireland.

Frontiers in Aging Neuroscience

|June 17, 2010

Summary

Aging brains exhibit increased microglial activation, impairing synaptic plasticity. Inhibiting this neuroinflammation in aged rats improved their ability to sustain long-term potentiation (LTP), suggesting a causal link.

Keywords:

cell-cell interaction inflammatory cytokines interleukin-1β (IL-1β)long-term potentiation microglial activation neuroinflammation

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Published on: December 8, 2017

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Last Updated: Jun 12, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

Published on: December 8, 2017

Area of Science:

Neuroscience
Immunology
Aging Research

Background:

Neuroinflammation, marked by microglial activation and elevated cytokines like interleukin-1beta (IL-1beta), is prevalent in neurodegenerative diseases and aging.
Age-related neuroinflammation can lead to impaired synaptic function and plasticity.

Purpose of the Study:

To review evidence linking age-related microglial activation to impaired synaptic plasticity, specifically long-term potentiation (LTP).
To explore the potential of inhibiting microglial activation as a therapeutic strategy for age-related cognitive decline.

Main Methods:

Review of existing literature on neuroinflammation, aging, and synaptic plasticity.
Analysis of studies investigating microglial activation markers in aged rodents.
Examination of data on the effects of anti-inflammatory agents on LTP in aged rats.

Main Results:

A decrease in the ability of aged rats to sustain hippocampal long-term potentiation (LTP) correlates with increased microglial activation.
Evidence suggests a causal relationship between age-related microglial activation and deficits in synaptic plasticity.
Agents that inhibit microglial activation were shown to improve LTP maintenance in aged rats.

Conclusions:

Age-related microglial activation is a significant contributor to impaired synaptic plasticity.
Targeting neuroinflammation by inhibiting microglial activation may offer a viable approach to enhance cognitive function in aging.