{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T07:19:48Z","timestamp":1791011988749,"version":"4.1.0"},"reference-count":90,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,6,21]],"date-time":"2013-06-21T00:00:00Z","timestamp":1371772800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:p>\n                    Degenerative dementia is mainly caused by\n                    <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                    lzheimer's disease and\/or cerebrovascular abnormalities. Disturbance of the intracellular calcium homeostasis is central to the pathophysiology of neurodegeneration. In\n                    <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                    lzheimer's disease, enhanced calcium load may be brought about by extracellular accumulation of amyloid\u2010\u03b2. Recent studies suggest that soluble forms facilitate influx through calcium\u2010conducting ion channels in the plasma membrane, leading to excitotoxic neurodegeneration. Calcium channel blockade attenuates amyloid\u2010\u03b2\u2010induced neuronal decline\n                    <jats:italic>in vitro<\/jats:italic>\n                    and is neuroprotective in animal models. Vascular dementia, on the other hand, is caused by cerebral hypoperfusion and may benefit from calcium channel blockade due to relaxation of the cerebral vasculature. Several calcium channel blockers have been tested in clinical trials of dementia and the outcome is heterogeneous. Nimodipine as well as nilvadipine prevent cognitive decline in some trials, whereas other calcium channel blockers failed. In trials with a positive outcome, BP reduction did not seem to play a role in preventing dementia, indicating a direct protecting effect on neurons. An optimization of calcium channel blockers for the treatment of dementia may involve an increase of selectivity for presynaptic calcium channels and an improvement of the affinity to the inactivated state. Novel low molecular weight compounds suitable for proof\u2010of\u2010concept studies are now available.\n                  <\/jats:p>","DOI":"10.1111\/bph.12240","type":"journal-article","created":{"date-parts":[[2013,5,3]],"date-time":"2013-05-03T06:25:31Z","timestamp":1367562331000},"page":"1203-1210","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":137,"title":["Calcium channel blockers and dementia"],"prefix":"10.1111","volume":"169","author":[{"given":"V","family":"Nimmrich","sequence":"first","affiliation":[{"name":"Neuroscience Research GPRD AbbVie GmbH  Ludwigshafen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Eckert","sequence":"additional","affiliation":[{"name":"Neurobiology Laboratory for Brain Aging and Mental Health Psychiatric University Clinics University of Basel  Basel 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