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000139442 0247_ $$2doi$$a10.1371/journal.pone.0182822
000139442 0247_ $$2pmid$$apmid:28796818
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000139442 041__ $$aEnglish
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000139442 1001_ $$0P:(DE-HGF)0$$aKraft, Peter$$b0$$eCorresponding author
000139442 245__ $$aHypercholesterolemia induced cerebral small vessel disease.
000139442 260__ $$aSan Francisco, California, US$$bPLOS$$c2017
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000139442 520__ $$aBackgroundWhile hypercholesterolemia plays a causative role for the development of ischemic stroke in large vessels, its significance for cerebral small vessel disease (CSVD) remains unclear. We thus aimed to understand the detailed relationship between hypercholesterolemia and CSVD using the well described Ldlr-/- mouse model.MethodsWe used Ldlr-/- mice (n = 16) and wild-type (WT) mice (n = 15) at the age of 6 and 12 months. Ldlr-/- mice develop high plasma cholesterol levels following a high fat diet. We analyzed cerebral capillaries and arterioles for intravascular erythrocyte accumulations, thrombotic vessel occlusions, blood-brain barrier (BBB) dysfunction and microbleeds.ResultsWe found a significant increase in the number of erythrocyte stases in 6 months old Ldlr-/- mice compared to all other groups (P < 0.05). Ldlr-/- animals aged 12 months showed the highest number of thrombotic occlusions while in WT animals hardly any occlusions could be observed (P < 0.001). Compared to WT mice, Ldlr-/- mice did not display significant gray matter BBB breakdown. Microhemorrhages were observed in one Ldlr-/- mouse that was 6 months old. Results did not differ when considering subcortical and cortical regions.ConclusionsIn Ldlr-/- mice, hypercholesterolemia is related to a thrombotic CSVD phenotype, which is different from hypertension-related CSVD that associates with a hemorrhagic CSVD phenotype. Our data demonstrate a relationship between hypercholesterolemia and the development of CSVD. Ldlr-/- mice appear to be an adequate animal model for research into CSVD.
000139442 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000139442 536__ $$0G:(DE-HGF)POF3-344$$a344 - Clinical and Health Care Research (POF3-344)$$cPOF3-344$$fPOF III$$x1
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000139442 650_7 $$2NLM Chemicals$$aReceptors, LDL
000139442 650_7 $$097C5T2UQ7J$$2NLM Chemicals$$aCholesterol
000139442 650_2 $$2MeSH$$aAnimals
000139442 650_2 $$2MeSH$$aBlood-Brain Barrier: physiopathology
000139442 650_2 $$2MeSH$$aBrain: physiopathology
000139442 650_2 $$2MeSH$$aCerebral Small Vessel Diseases: blood
000139442 650_2 $$2MeSH$$aCerebral Small Vessel Diseases: etiology
000139442 650_2 $$2MeSH$$aCerebral Small Vessel Diseases: genetics
000139442 650_2 $$2MeSH$$aCerebral Small Vessel Diseases: physiopathology
000139442 650_2 $$2MeSH$$aCholesterol: blood
000139442 650_2 $$2MeSH$$aDiet, High-Fat
000139442 650_2 $$2MeSH$$aDisease Models, Animal
000139442 650_2 $$2MeSH$$aHypercholesterolemia: blood
000139442 650_2 $$2MeSH$$aHypercholesterolemia: complications
000139442 650_2 $$2MeSH$$aHypercholesterolemia: genetics
000139442 650_2 $$2MeSH$$aHypercholesterolemia: physiopathology
000139442 650_2 $$2MeSH$$aMale
000139442 650_2 $$2MeSH$$aMice
000139442 650_2 $$2MeSH$$aMice, Knockout
000139442 650_2 $$2MeSH$$aReceptors, LDL: genetics
000139442 7001_ $$0P:(DE-HGF)0$$aSchuhmann, Michael K$$b1
000139442 7001_ $$0P:(DE-2719)2813207$$aGarz, Cornelia$$b2$$udzne
000139442 7001_ $$0P:(DE-2719)2813348$$aJandke, Solveig$$b3$$udzne
000139442 7001_ $$0P:(DE-HGF)0$$aUrlaub, Daniela$$b4
000139442 7001_ $$0P:(DE-HGF)0$$aMencl, Stine$$b5
000139442 7001_ $$0P:(DE-HGF)0$$aZernecke, Alma$$b6
000139442 7001_ $$0P:(DE-2719)2260426$$aHeinze, Hans-Jochen$$b7$$udzne
000139442 7001_ $$0P:(DE-HGF)0$$aCarare, Roxana O$$b8
000139442 7001_ $$0P:(DE-HGF)0$$aKleinschnitz, Christoph$$b9
000139442 7001_ $$0P:(DE-2719)2812631$$aSchreiber, Stefanie$$b10$$eLast author$$udzne
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000139442 8564_ $$uhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0182822
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