Currently used broad spectrum therapy with glucocorticoids (e.g., triamcinolone), and targeted therapies with monoclonal antibodies (e.g., dupilumab, tralokinumab) blocking IL-4 receptor, or small molecule inhibitors targeting intracellular signaling intermediates, such as Janus Kinases (JAKs; e.g., upadacitinib and abrocitinib), Phosphodiesterase 4 (PDE4; e.g., crisaborole), and calcineurin (e.g., tacrolimus, pimecrolimus), only partially inhibit inflammatory signaling responsible for AD development and persistence2,5–7. This evidence concerns the gene PDE4A and Alzheimer disease.