These receptor interactions influence signals that regulate food intake and fullness in research models
moreover, crossing SOD1 G93A mice with mice overexpressing Nrf2 selectively in astrocytes significantly delayed disease onset and extended survival, thus reversing the toxicity of astrocytes expressing human SOD1 G93A mutation to co-cultured MNs [266, 267]
Image: Peter Dazeley/Getty Images About the Author Marygrace Taylor, Health Writer About the Reviewer Pieter Cohen, MD, Contributor Disclaimer: As a service to our readers, Harvard Health Publishing provides access to our library of archived content
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