Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSPJUSTO, Alberto Fernando OliveiraTOSCANO, Eliana Cristina de BritoFARIAS-ITAO, Daniela SouzaSUEMOTO, Claudia Kimie2023-06-212023-06-212023LIFE SCIENCES, v.320, article ID 121570, 10p, 20230024-3205https://observatorio.fm.usp.br/handle/OPI/53784Alzheimer's disease (AD) is the most frequent cause of dementia worldwide. The etiology of AD is partially explained by the deposition of beta-amyloid in the brain. Despite extensive research on the pathogenesis of AD, the current treatments are ineffective. Here, we systematically reviewed studies that investigated whether phos-phodiesterase 5 inhibitors (PDE5i) are efficient in reducing the beta-amyloid load in hippocampi and improving cognitive decline in rodent models with beta-amyloid accumulation. We identified ten original studies, which used rodent models with beta-amyloid accumulation, were treated with PDE5i, and beta-amyloid was measured in the hippocampi. PDE5i was efficient in reducing the beta-amyloid levels, except for one study that exclusively used female rodents and the treatment did not affect beta-amyloid levels. Interestingly, PDE5i prevented cognitive decline in all studies. This study supports the potential therapeutic use of PDE5i for the reduction of the beta-amyloid load in hippocampi and cognitive decline. However, we highlight the importance of conducting additional experimental studies to evaluate the PDE5i-related molecular mechanisms involved in beta-amyloid removal in male and female animals.engrestrictedAccessAlzheimer?s diseasePhosphodiesterase 5 inhibitorsBeta-amyloidelement-binding proteinapp/ps1 transgenic miceneuronal cell-deathprecursor proteinbetasildenafilbrainexpressionclearancedementiaarticleCopyright PERGAMON-ELSEVIER SCIENCE LTD10.1016/j.lfs.2023.121570Medicine, Research & ExperimentalPharmacology & Pharmacy1879-0631