For instance, cross-bleeding of mice expressing Swedish APP with diabetic mice (either ob/ob or NSY mice) revealed that a variety of neuropathology, including cerebrovascular inflammation and severe amyloid angiopathy, was exacerbated, while the diabetic phenotypes in cross-bred mice are accelerated compared with those of monogenic mice, suggesting that AD and diabetes induce mutual disease progression.54 Relevant to PD, diet-induced obesity accelerates the onset of “terminal phenotypes” in αS transgenic mice characterized by increased amyloid-like deposits and premature αS pathology.55 This evidence concerns the gene APP and Parkinson disease.