{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T06:42:24Z","timestamp":1792392144241,"version":"4.4.0"},"reference-count":63,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,18]],"date-time":"2026-10-18T00:00:00Z","timestamp":1792281600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,18]],"date-time":"2026-10-18T00:00:00Z","timestamp":1792281600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Anim Models and Exp Med"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Post\u2010stroke cognitive impairment (PSCI) is a major cause of long\u2010term disability after ischemic stroke, yet its mechanisms remain incompletely explained by infarct volume, lesion location, or conventional vascular risk factors alone. Animal models are indispensable for clarifying how ischemic injury evolves into delayed cognitive dysfunction and for determining which mechanisms are experimentally tractable, reproducible, and translationally relevant. This review examines PSCI from a neurovascular trafficking perspective, focusing on how laboratory animal models can be used to investigate secretory pathway stress, endolysosomal dysfunction, autophagy\u2010lysosomal flux, extracellular vesicle signaling, blood\u2013brain barrier disruption, glial reactivity, myelin debris clearance, white matter injury, and cognition\u2010relevant behavioral phenotypes. Rodent models of transient or permanent middle cerebral artery occlusion, photothrombotic stroke, embolic stroke, chronic cerebral hypoperfusion, bilateral carotid artery stenosis, and subcortical white\u2010matter injury each reproduce selected components of the human PSCI spectrum. No single model fully captures the temporal, vascular, cellular, and cognitive complexity of human PSCI; therefore, model selection should be driven by the mechanistic question, disease phase, vascular pathology, cellular compartment, cognitive domain, and welfare burden under investigation. The central argument is not that neurovascular trafficking failure is already a proven causal pathway, but that well\u2010designed animal studies can test, refine, or falsify this hypothesis. Future studies should integrate model validity, translational rigor, and welfare refinement through longitudinal cognitive testing, multimodal imaging, cell\u2010specific molecular profiling, extracellular vesicle phenotyping, intervention\u2010based validation, randomization, blinding, sample\u2010size justification, humane endpoints, perioperative care, and transparent reporting.<\/jats:p>","DOI":"10.1002\/ame2.70315","type":"journal-article","created":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T05:57:32Z","timestamp":1792389452000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Animal models for investigating post\u2010stroke cognitive impairment: A neurovascular trafficking perspective"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6214-7767","authenticated-orcid":false,"given":"Pratchaya","family":"Kaewkaen","sequence":"first","affiliation":[{"name":"Animal Cognitive 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