Strikingly, treatment with Glyz to inhibit HMGB-1 activity was able to markedly enhance relaxation in models of acute HHcy or after a 4-week AD, reduced expression of nitrotyrosine and TNFα, upregulated eNOS levels and restored levels of HMGB-1 in blood vessels to those of rabbits fed a CD. The gene discussed is HMGB1; the disease is Alzheimer disease.