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By directly linking postmortem human <jats:styled-content style=\"fixed-case\">MRI<\/jats:styled-content> sequences with histological features of periventricular tissue, we show that substantial lateral ventricle surface gliosis is associated with ventriculomegaly. To examine whether loss of ependymal cell coverage resulting in ventricle surface glial scarring can lead directly to ventricle enlargement independent of any other injury or degenerative loss, we modeled in mice the glial scarring found along the lateral ventricle surface in aged humans. Neuraminidase, which cleaves glycosidic linkages of apical adherens junction proteins, was administered intracerebroventricularly to denude areas of ependymal cells. Substantial ependymal cell loss resulted in reactive gliosis rather than stem cell\u2010mediated regenerative repair of the ventricle lining, and the gliotic regions showed morphologic and phenotypic characteristics similar to those found in aged humans. Increased levels of aquaporin\u20104, indicative of edema, observed in regions of periventricular gliosis in human tissue were also replicated in our mouse model. 3<jats:styled-content style=\"fixed-case\">D<\/jats:styled-content> modeling together with volume measurements revealed that mice with ventricle surface scarring developed expanded ventricles, independent of neurodegeneration. Through a comprehensive, comparative analysis of the lateral ventricles and associated periventricular tissue in aged humans and mouse, followed by modeling of surface gliosis in mice, we have demonstrated a direct link between lateral ventricle surface gliosis and ventricle enlargement. These studies highlight the importance of maintaining an intact ependymal cell lining throughout aging.<\/jats:p>","DOI":"10.1111\/acel.12184","type":"journal-article","created":{"date-parts":[[2013,12,17]],"date-time":"2013-12-17T10:48:41Z","timestamp":1387277321000},"page":"340-350","source":"Crossref","is-referenced-by-count":62,"title":["Ventriculomegaly associated with ependymal gliosis and declines in barrier integrity in the aging human and mouse brain"],"prefix":"10.1111","volume":"13","author":[{"given":"Brett A.","family":"Shook","sequence":"first","affiliation":[{"name":"Department of Physiology and Neurobiology University of Connecticut Storrs CT 06269\u20103156 USA"},{"name":"Stem Cell Institute University of Connecticut Storrs CT 06269\u20103156 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica B.","family":"Lennington","sequence":"additional","affiliation":[{"name":"Department of Physiology and Neurobiology University of Connecticut Storrs CT 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