{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T18:36:30Z","timestamp":1785868590299,"version":"3.56.0"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","license":[{"start":{"date-parts":[[2024,7,1]],"date-time":"2024-07-01T00:00:00Z","timestamp":1719792000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Cerebral small vessel disease is a common cause of vascular cognitive impairment and dementia. There is an urgent need for preventative treatments for vascular cognitive impairment and dementia, and reducing vascular dysfunction may provide a therapeutic route. Here, we investigate whether the chronic administration of nimodipine, a central nervous system-selective dihydropyridine calcium channel blocking agent, protects vascular, metabolic, and cognitive function in an animal model of cerebral small vessel disease, the spontaneously hypertensive stroke-prone rat.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>Male spontaneously hypertensive stroke-prone rats were randomly allocated to receive either a placebo (n=24) or nimodipine (n=24) diet between 3 and 6 months of age. Animals were examined daily for any neurological deficits, and vascular function was assessed in terms of neurovascular and neurometabolic coupling at 3 and 6 months of age, and cerebrovascular reactivity at 6 months of age. Cognitive function was evaluated using the novel object recognition test at 6 months of age.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              Six untreated control animals were terminated prematurely due to strokes, including one due to seizure, but no treated animals experienced strokes and so had a higher survival (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.0088). Vascular function was significantly impaired with disease progression, but nimodipine treatment partially preserved neurovascular coupling and neurometabolic coupling, indicated by larger (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              &lt;0.001) and more prompt responses (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              &lt;0.01), and less habituation upon repeated stimulation (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              &lt;0.01). Also, animals treated with nimodipine showed greater cerebrovascular reactivity, indicated by larger dilation of arterioles (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.015) and an increase in blood flow velocity (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.001). This protection of vascular and metabolic function achieved by nimodipine treatment was associated with better cognitive function (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              &lt;0.001) in the treated animals.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>Chronic treatment with nimodipine protects from strokes, and vascular and cognitive deficits in spontaneously hypertensive stroke-prone rat. Nimodipine may provide an effective preventive treatment for stroke and cognitive decline in cerebral small vessel disease.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/strokeaha.124.047154","type":"journal-article","created":{"date-parts":[[2024,6,11]],"date-time":"2024-06-11T09:01:38Z","timestamp":1718096498000},"page":"1914-1922","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":16,"title":["Nimodipine Protects Vascular and Cognitive Function in an Animal Model of Cerebral Small Vessel Disease"],"prefix":"10.1161","volume":"55","author":[{"given":"Zhiyuan","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Neuroinflammation, UCL Queen Square Institute of Neurology (Z.Y., Y.X., C.C., K.C., M.S., K.J.S.), University College London, United 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of Neurology (Z.Y., Y.X., C.C., K.C., M.S., K.J.S.), University College London, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9932-4923","authenticated-orcid":true,"given":"Katerina","family":"Cabolis","sequence":"additional","affiliation":[{"name":"Department of Neuroinflammation, UCL Queen Square Institute of Neurology (Z.Y., Y.X., C.C., K.C., M.S., K.J.S.), University College London, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4050-7477","authenticated-orcid":true,"given":"Marija","family":"Sajic","sequence":"additional","affiliation":[{"name":"Department of Neuroinflammation, UCL Queen Square Institute of Neurology (Z.Y., Y.X., C.C., K.C., M.S., K.J.S.), University College London, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2074-1861","authenticated-orcid":true,"given":"David 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