Hainsworth, Atticus H.Allan, Stuart M.Boltze, JohannesCunningham, CatrionaFarris, ChadHead, ElizabethIhara, MasafumiIsaacs, Jeremy D.Kalaria, Raj N.Lesnik Oberstein, Saskia A. M. J.Moss, Mark B.Nitzsche, BjörnRosenberg, Gary A.Rutten, Julie W.Salkovic-Petrisic, MelitaTroen, Aron M.2017-02-182017Hainsworth, A. H., S. M. Allan, J. Boltze, C. Cunningham, C. Farris, E. Head, M. Ihara, et al. 2017. “Translational models for vascular cognitive impairment: a review including larger species.” BMC Medicine 15 (1): 16. doi:10.1186/s12916-017-0793-9. http://dx.doi.org/10.1186/s12916-017-0793-9.1741-7015http://nrs.harvard.edu/urn-3:HUL.InstRepos:30370943Background: Disease models are useful for prospective studies of pathology, identification of molecular and cellular mechanisms, pre-clinical testing of interventions, and validation of clinical biomarkers. Here, we review animal models relevant to vascular cognitive impairment (VCI). A synopsis of each model was initially presented by expert practitioners. Synopses were refined by the authors, and subsequently by the scientific committee of a recent conference (International Conference on Vascular Dementia 2015). Only peer-reviewed sources were cited. Methods: We included models that mimic VCI-related brain lesions (white matter hypoperfusion injury, focal ischaemia, cerebral amyloid angiopathy) or reproduce VCI risk factors (old age, hypertension, hyperhomocysteinemia, high-salt/high-fat diet) or reproduce genetic causes of VCI (CADASIL-causing Notch3 mutations). Conclusions: We concluded that (1) translational models may reflect a VCI-relevant pathological process, while not fully replicating a human disease spectrum; (2) rodent models of VCI are limited by paucity of white matter; and (3) further translational models, and improved cognitive testing instruments, are required.en-USVascular dementiaVascular cognitive impairmentVCIDExperimental modelsIn vivo modelsTranslational modelsJournal Article2017-02-1810.1186/s12916-017-0793-9