Inhibition of neuroinflammatory nitric oxide signaling suppresses glycation and prevents neuronal dysfunction in mouse prion disease

Significance We present evidence that alleviating nitrergic stress during early phases of neurodegeneration reduces neuroinflammatory posttranslational nitric oxide signaling and glycation-assisted dysfunction in the hippocampus prion-diseased mice, a mechanism which might be applicable to other protein-misfolding neurodegenerative conditions. confirmed pharmacological suppression activity formation advanced glycation end-products, diminishes prion protein misfolding, averts neuronal dysfunction. This intervention could an approach diminish detrimental effects seen highlights as putative targets for disease-modifying treatments. The correlation between misfolding—as reported several misfolding proteins—links NO neuroprotective following NOS inhibition.