01444nas a2200289   4500000000100000000000100001008004100002260001500043653002600058653002400084653002100108653004100129653002300170653001600193100001900209700002300228700001700251700001600268700002300284700002700307245009900334856004700433300000600480490000700486520064700493022001401140       2026                            d  c2026-01-0610aAlzheimer’s disease10aBlood-Brain Barrier10adisease modeling10ahuman induced pluripotent stem cells10aNeurovascular unit10aOrgan-chips1 aAndrew N. Shen1 aKatelin S. Matazel1 aW. Drew Gill1 aLorna Ewart1 aRandy S. Daughters1 aHector Rosas-Hernandez00aModeling neurovascular dysfunction in Alzheimer’s disease using an isogenic brain-chip model  uhttps://doi.org/10.1186/s12987-025-00708-y  a10 v233 aThe pathology of Alzheimer’s Disease (AD) is characterized by aggregates of amyloid beta (Aβ) peptides and neurofibrillary tau tangles. Increased blood-brain barrier (BBB) permeability and reduced Aβ clearance, which signal neurovascular dysfunction, have also been proposed as early markers of AD. Despite intense scrutiny, the mechanisms of AD remain elusive and novel treatments that address core symptoms of dementia are limited. New alternative methods (NAMs) aim to develop in-vitro translational models that recapitulate human pathology more accurately than previous models and could contribute to the development of new therapies.  a2045-8118