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000137854 037__ $$aDZNE-2020-04176
000137854 041__ $$aEnglish
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000137854 1001_ $$0P:(DE-HGF)0$$aJadavji, Nafisa M$$b0$$eCorresponding author
000137854 245__ $$aElevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil-DNA glycosylase impair learning in a mouse model of vascular cognitive impairment.
000137854 260__ $$aAmsterdam$$bElsevier$$c2015
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000137854 520__ $$aDietary deficiencies in folic acid result in elevated levels of plasma homocysteine, which has been associated with the development of dementia and other neurodegenerative disorders. Previously, we have shown that elevated levels of plasma homocysteine in mice deficient for a DNA repair enzyme, uracil-DNA glycosylase (UNG), result in neurodegeneration. The goal of this study was to evaluate how deficiencies in folic acid and UNG along with elevated levels of homocysteine affect vascular cognitive impairment, via chronic hypoperfursion in an animal model. Ung(+/+) and Ung(-/-) mice were placed on either control (CD) or folic acid deficient (FADD) diets. Six weeks later, the mice either underwent implantation of microcoils around both common carotid arteries. Post-operatively, behavioral tests began at 3-weeks, angiography was measured after 5-weeks using MRI to assess vasculature and at completion of study plasma and brain tissue was collected for analysis. Learning impairments in the Morris water maze (MWM) were observed only in hypoperfused Ung(-/-) FADD mice and these mice had significantly higher plasma homocysteine concentrations. Interestingly, Ung(+/+) FADD produced significant remodeling of the basilar artery and arterial vasculature. Increased expression of GFAP was observed in the dentate gyrus of Ung(-/-) hypoperfused and FADD sham mice. Chronic hypoperfusion resulted in increased cortical MMP-9 protein levels of FADD hypoperfused mice regardless of genotypes. These results suggest that elevated levels of homocysteine only, as a result of dietary folic acid deficiency, don't lead to memory impairments and neurobiochemical changes. Rather a combination of either chronic hypoperfusion or UNG deficiency is required.
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000137854 650_7 $$2NLM Chemicals$$aGlial Fibrillary Acidic Protein
000137854 650_7 $$2NLM Chemicals$$aNerve Tissue Proteins
000137854 650_7 $$2NLM Chemicals$$aglial fibrillary astrocytic protein, mouse
000137854 650_7 $$00LVT1QZ0BA$$2NLM Chemicals$$aHomocysteine
000137854 650_7 $$0EC 3.2.2.-$$2NLM Chemicals$$aUracil-DNA Glycosidase
000137854 650_7 $$0EC 3.4.24.35$$2NLM Chemicals$$aMatrix Metalloproteinase 9
000137854 650_7 $$0EC 3.4.24.35$$2NLM Chemicals$$aMmp9 protein, mouse
000137854 650_2 $$2MeSH$$aAnimals
000137854 650_2 $$2MeSH$$aBasilar Artery: pathology
000137854 650_2 $$2MeSH$$aBasilar Artery: physiopathology
000137854 650_2 $$2MeSH$$aBrain: blood supply
000137854 650_2 $$2MeSH$$aBrain: pathology
000137854 650_2 $$2MeSH$$aBrain: physiopathology
000137854 650_2 $$2MeSH$$aCarotid Artery Diseases
000137854 650_2 $$2MeSH$$aCerebrovascular Disorders: pathology
000137854 650_2 $$2MeSH$$aCerebrovascular Disorders: physiopathology
000137854 650_2 $$2MeSH$$aChronic Disease
000137854 650_2 $$2MeSH$$aCognition Disorders: pathology
000137854 650_2 $$2MeSH$$aCognition Disorders: physiopathology
000137854 650_2 $$2MeSH$$aDiet
000137854 650_2 $$2MeSH$$aDisease Models, Animal
000137854 650_2 $$2MeSH$$aFemale
000137854 650_2 $$2MeSH$$aFolic Acid Deficiency: pathology
000137854 650_2 $$2MeSH$$aFolic Acid Deficiency: physiopathology
000137854 650_2 $$2MeSH$$aGlial Fibrillary Acidic Protein
000137854 650_2 $$2MeSH$$aGliosis: pathology
000137854 650_2 $$2MeSH$$aGliosis: physiopathology
000137854 650_2 $$2MeSH$$aHomocysteine: blood
000137854 650_2 $$2MeSH$$aLearning Disabilities: pathology
000137854 650_2 $$2MeSH$$aLearning Disabilities: physiopathology
000137854 650_2 $$2MeSH$$aMale
000137854 650_2 $$2MeSH$$aMatrix Metalloproteinase 9: metabolism
000137854 650_2 $$2MeSH$$aMaze Learning: physiology
000137854 650_2 $$2MeSH$$aMice, Inbred C57BL
000137854 650_2 $$2MeSH$$aMice, Knockout
000137854 650_2 $$2MeSH$$aNerve Tissue Proteins: metabolism
000137854 650_2 $$2MeSH$$aRandom Allocation
000137854 650_2 $$2MeSH$$aUracil-DNA Glycosidase: deficiency
000137854 650_2 $$2MeSH$$aUracil-DNA Glycosidase: genetics
000137854 7001_ $$aFarr, Tracy D$$b1
000137854 7001_ $$aLips, Janet$$b2
000137854 7001_ $$aKhalil, Ahmed A$$b3
000137854 7001_ $$aBoehm-Sturm, Philipp$$b4
000137854 7001_ $$0P:(DE-HGF)0$$aFoddis, Marco$$b5
000137854 7001_ $$aHarms, Christoph$$b6
000137854 7001_ $$0P:(DE-HGF)0$$aFüchtemeier, Martina$$b7
000137854 7001_ $$0P:(DE-2719)2810838$$aDirnagl, Ulrich$$b8$$eLast author$$udzne
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