What is it about?
Bioaccumulation of amyloid beta (AB) peptides is implicated in Alzheimer’s disease. Animal models over-expressing AB show memory deficits. Hippocampal sharp-wave ripples have been implicated in memory consolidation. Disruption of these same high frequency oscillations produces memory deficits. Compounds that decrease tonic inhibition mediated by a5 type GABA receptors improve memory function in healthy rodents. It is not known whether these compounds modulate ripples in vivo. We now show for the first time that administration of a putative cognitive enhancer selective for a5 type GABA receptors increases peak ripple amplitudes in wild type adult rats but has no effect on peak ripple amplitudes in adult TgF344-AD rats which show elevated plasma concentrations of AB42 and AB40.
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Why is it important?
This important novel finding has far reaching translational implications for future studies using pharmacologic as well as deep brain stimulation methods to restore the ripple amplitude deficits observed in this preclinical animal model of Alzheimer's disease necessary to move these findings from the bench to the bedside.
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This page is a summary of: Prodromal dysfunction of α5GABA-A receptor modulated hippocampal ripples in Alzheimer’s disease, May 2021, Cold Spring Harbor Laboratory Press,
DOI: 10.1101/2021.05.10.443512.
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