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

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Published on: March 23, 2011

Brain ageing changes proteoglycan sulfation, rendering perineuronal nets more inhibitory.

Simona Foscarin¹, Ruma Raha-Chowdhury¹, James W Fawcett^1,2

¹John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0PY, United Kingdom.

|June 29, 2017

Summary

Aging brains show altered chondroitin sulfate (CS) proteoglycans in perineuronal nets (PNNs), increasing inhibitory C4S and decreasing permissive C6S, which impairs plasticity and memory.

Keywords:

aging glycosaminoglycans perineuronal net plasticity sulfation

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Isolation of Intermediate Filament Proteins from Multiple Mouse Tissues to Study Aging-associated Post-translational Modifications

Isolation of Intermediate Filament Proteins from Multiple Mouse Tissues to Study Aging-associated Post-translational Modifications

Published on: May 18, 2017

Area of Science:

Neuroscience
Biochemistry
Aging Research

Background:

Perineuronal nets (PNNs) in the central nervous system (CNS) contain chondroitin sulfate (CS) proteoglycans, regulating plasticity and memory.
Altered PNNs are implicated in cognitive decline associated with aging and Alzheimer's disease.
CS proteoglycan GAG chains, sulfated as C4S or C6S, differentially affect neuronal plasticity, with C4S being inhibitory and C6S permissive.

Purpose of the Study:

To investigate age-related changes in CS-GAG sulfation within rat brain PNNs.
To determine if these changes correlate with memory decline in aging rats.

Main Methods:

Immunohistochemistry was used to analyze C4S and C6S levels in rat brain PNNs at different ages (3, 12, and 18 months).
Glycosaminoglycans (GAGs) were extracted from brain PNNs for sulfation analysis.
Axon growth inhibition assays were performed on PNN GAGs from different age groups.

Main Results:

A progressive increase in C4S and a decrease in C6S were observed in PNNs from 3 to 18 months.
Extracted PNN GAGs showed a reduced C6S content and an increased C4S/C6S ratio in aged rats (12 and 18 months).
GAGs from aged PNNs exhibited greater inhibition of axon growth compared to those from younger rats.

Conclusions:

Aging in rats is associated with a shift in PNN GAG sulfation towards a more inhibitory profile (increased C4S, decreased C6S).
This altered PNN GAG composition likely contributes to reduced neuronal plasticity and memory impairment in aged brains.
The findings suggest PNN GAG sulfation as a potential target for interventions against age-related cognitive decline.