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However, little is known about the severe pathological condition and dementia that occur as a result of the comorbid occurrence of this vascular risk factor and <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>beta toxicity. Clinical studies have indicated that small ischemic lesions in the striatum are particularly important in generating dementia in combination with minor amyloid lesions. These cognitive deficits are highly likely to be caused by changes in the cortex. In this study, we examined the viability and morphological changes in microglial and neuronal cells, gap junction proteins (connexin43) and neuritic\/axonal retraction (<jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>er <jats:styled-content style=\"fixed-case\">K<\/jats:styled-content>inase) in the striatum and cerebral cortex using a comorbid rat model of striatal injections of endothelin\u20101 (<jats:styled-content style=\"fixed-case\">ET<\/jats:styled-content>1) and <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>beta toxicity. The results demonstrated ventricular enlargement, striatal atrophy, substantial increases in \u03b2\u2010amyloid, ramified microglia and increases in neuritic retraction in the combined models of stroke and <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>beta toxicity. Changes in connexin43 occurred equally in both groups of <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>beta\u2010treated rats, with and without focal ischemia. Although previous behavioral tests demonstrated impairment in memory and learning, the visual discrimination radial maze task did not show significant difference, suggesting the cognitive impairment in these models is not related to damage to the dorsolateral striatum. These results suggest an insight into the relationship between cortical\/striatal atrophy, pathology and functional impairment.<\/jats:p>","DOI":"10.1111\/bpa.12149","type":"journal-article","created":{"date-parts":[[2014,4,11]],"date-time":"2014-04-11T13:38:37Z","timestamp":1397223517000},"page":"24-32","source":"Crossref","is-referenced-by-count":31,"title":["Comorbid Rat Model of Ischemia and \u03b2\u2010Amyloid Toxicity: Striatal and Cortical Degeneration"],"prefix":"10.1111","volume":"25","author":[{"given":"Zareen","family":"Amtul","sequence":"first","affiliation":[{"name":"CIHR Group on Vascular Cognitive Impairment Department of Anatomy and Cell Biology Western University  London ON Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shawn N.","family":"Whitehead","sequence":"additional","affiliation":[{"name":"CIHR Group on Vascular Cognitive Impairment Department of Anatomy and Cell Biology Western University  London ON Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robin J.","family":"Keeley","sequence":"additional","affiliation":[{"name":"Canadian Centre for Behavioural Neuroscience Department of Neuroscience University of Lethbridge  Lethbridge AB Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John","family":"Bechberger","sequence":"additional","affiliation":[{"name":"Department of Cellular and Physiological Sciences The Life Sciences Institute University of British Columbia  Vancouver BC Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alicia L.","family":"Fisher","sequence":"additional","affiliation":[{"name":"Canadian Centre for Behavioural Neuroscience Department of Neuroscience University of Lethbridge  Lethbridge AB Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert J.","family":"McDonald","sequence":"additional","affiliation":[{"name":"Canadian Centre for Behavioural Neuroscience Department 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