The pathological sequelae of AD, neurodegeneration, synaptic dysregulation and intracellular and extracellular protein accumulation, are accompanied, in both sporadic and Mendelian AD, by the distinct post-translational processing of amyloid precursor protein and its accumulation, which triggers cyclic AMP hydrolysis that is sensitive to PDE antagonism [40,41]. The gene discussed is ALDH7A1; the disease is Alzheimer disease.