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Despite this warning research regarding AD has long been focused on the amyloid cascade hypothesis and strategies to prevent and/or remove plaques [2,8]

In vitro studies revealed a dramatic increase in the number of cells expressing the intercellular adhesion molecule CD34 and an increase in the number of CD31 + cells with active esterase under the direct action of GLP-1, suggesting that endothelial progenitor cells expressing CD31 and CD34 endothelial progenitor cell markers may be targets of GLP-1 and participate in the regeneration process of damaged endothelium in emphysematous mice with heterotrophic insulin, 47 and thus in airway remodeling