Home > Publications Database > Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil-DNA glycosylase impair learning in a mouse model of vascular cognitive impairment. > print

001     137854
005     20240321220328.0
024 7 _ |a 10.1016/j.bbr.2015.01.040
|2 doi
024 7 _ |a pmid:25655513
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024 7 _ |a 0166-4328
|2 ISSN
024 7 _ |a 1872-7549
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024 7 _ |a altmetric:52784158
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037 _ _ |a DZNE-2020-04176
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Jadavji, Nafisa M
|0 P:(DE-HGF)0
|b 0
|e Corresponding author
245 _ _ |a Elevated levels of plasma homocysteine, deficiencies in dietary folic acid and uracil-DNA glycosylase impair learning in a mouse model of vascular cognitive impairment.
260 _ _ |a Amsterdam
|c 2015
|b Elsevier
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2015-04-01
336 7 _ |a article
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336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Dietary 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.
536 _ _ |a 344 - Clinical and Health Care Research (POF3-344)
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542 _ _ |i 2015-04-01
|2 Crossref
|u https://www.elsevier.com/tdm/userlicense/1.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Glial Fibrillary Acidic Protein
|2 NLM Chemicals
650 _ 7 |a Nerve Tissue Proteins
|2 NLM Chemicals
650 _ 7 |a glial fibrillary astrocytic protein, mouse
|2 NLM Chemicals
650 _ 7 |a Homocysteine
|0 0LVT1QZ0BA
|2 NLM Chemicals
650 _ 7 |a Uracil-DNA Glycosidase
|0 EC 3.2.2.-
|2 NLM Chemicals
650 _ 7 |a Matrix Metalloproteinase 9
|0 EC 3.4.24.35
|2 NLM Chemicals
650 _ 7 |a Mmp9 protein, mouse
|0 EC 3.4.24.35
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Basilar Artery: pathology
|2 MeSH
650 _ 2 |a Basilar Artery: physiopathology
|2 MeSH
650 _ 2 |a Brain: blood supply
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Brain: physiopathology
|2 MeSH
650 _ 2 |a Carotid Artery Diseases
|2 MeSH
650 _ 2 |a Cerebrovascular Disorders: pathology
|2 MeSH
650 _ 2 |a Cerebrovascular Disorders: physiopathology
|2 MeSH
650 _ 2 |a Chronic Disease
|2 MeSH
650 _ 2 |a Cognition Disorders: pathology
|2 MeSH
650 _ 2 |a Cognition Disorders: physiopathology
|2 MeSH
650 _ 2 |a Diet
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Folic Acid Deficiency: pathology
|2 MeSH
650 _ 2 |a Folic Acid Deficiency: physiopathology
|2 MeSH
650 _ 2 |a Glial Fibrillary Acidic Protein
|2 MeSH
650 _ 2 |a Gliosis: pathology
|2 MeSH
650 _ 2 |a Gliosis: physiopathology
|2 MeSH
650 _ 2 |a Homocysteine: blood
|2 MeSH
650 _ 2 |a Learning Disabilities: pathology
|2 MeSH
650 _ 2 |a Learning Disabilities: physiopathology
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Matrix Metalloproteinase 9: metabolism
|2 MeSH
650 _ 2 |a Maze Learning: physiology
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Knockout
|2 MeSH
650 _ 2 |a Nerve Tissue Proteins: metabolism
|2 MeSH
650 _ 2 |a Random Allocation
|2 MeSH
650 _ 2 |a Uracil-DNA Glycosidase: deficiency
|2 MeSH
650 _ 2 |a Uracil-DNA Glycosidase: genetics
|2 MeSH
700 1 _ |a Farr, Tracy D
|b 1
700 1 _ |a Lips, Janet
|b 2
700 1 _ |a Khalil, Ahmed A
|b 3
700 1 _ |a Boehm-Sturm, Philipp
|b 4
700 1 _ |a Foddis, Marco
|0 P:(DE-HGF)0
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700 1 _ |a Harms, Christoph
|b 6
700 1 _ |a Füchtemeier, Martina
|0 P:(DE-HGF)0
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700 1 _ |a Dirnagl, Ulrich
|0 P:(DE-2719)2810838
|b 8
|e Last author
|u dzne
773 1 8 |a 10.1016/j.bbr.2015.01.040
|b : Elsevier BV, 2015-04-01
|p 215-226
|3 journal-article
|2 Crossref
|t Behavioural Brain Research
|v 283
|y 2015
|x 0166-4328
773 _ _ |a 10.1016/j.bbr.2015.01.040
|g Vol. 283, p. 215 - 226
|0 PERI:(DE-600)2013604-3
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|p 215-226
|t Behavioural brain research
|v 283
|y 2015
|x 0166-4328
856 4 _ |u https://pub.dzne.de/record/137854/files/DZNE-2020-04176_Restricted.pdf
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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