% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Jadavji:137854,
      author       = {Jadavji, Nafisa M and Farr, Tracy D and Lips, Janet and
                      Khalil, Ahmed A and Boehm-Sturm, Philipp and Foddis, Marco
                      and Harms, Christoph and Füchtemeier, Martina and Dirnagl,
                      Ulrich},
      title        = {{E}levated levels of plasma homocysteine, deficiencies in
                      dietary folic acid and uracil-{DNA} glycosylase impair
                      learning in a mouse model of vascular cognitive impairment.},
      journal      = {Behavioural brain research},
      volume       = {283},
      issn         = {0166-4328},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-04176},
      pages        = {215-226},
      year         = {2015},
      abstract     = {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.},
      keywords     = {Animals / Basilar Artery: pathology / Basilar Artery:
                      physiopathology / Brain: blood supply / Brain: pathology /
                      Brain: physiopathology / Carotid Artery Diseases /
                      Cerebrovascular Disorders: pathology / Cerebrovascular
                      Disorders: physiopathology / Chronic Disease / Cognition
                      Disorders: pathology / Cognition Disorders: physiopathology
                      / Diet / Disease Models, Animal / Female / Folic Acid
                      Deficiency: pathology / Folic Acid Deficiency:
                      physiopathology / Glial Fibrillary Acidic Protein / Gliosis:
                      pathology / Gliosis: physiopathology / Homocysteine: blood /
                      Learning Disabilities: pathology / Learning Disabilities:
                      physiopathology / Male / Matrix Metalloproteinase 9:
                      metabolism / Maze Learning: physiology / Mice, Inbred C57BL
                      / Mice, Knockout / Nerve Tissue Proteins: metabolism /
                      Random Allocation / Uracil-DNA Glycosidase: deficiency /
                      Uracil-DNA Glycosidase: genetics / Glial Fibrillary Acidic
                      Protein (NLM Chemicals) / Nerve Tissue Proteins (NLM
                      Chemicals) / glial fibrillary astrocytic protein, mouse (NLM
                      Chemicals) / Homocysteine (NLM Chemicals) / Uracil-DNA
                      Glycosidase (NLM Chemicals) / Matrix Metalloproteinase 9
                      (NLM Chemicals) / Mmp9 protein, mouse (NLM Chemicals)},
      cin          = {AG Dirnagl},
      ddc          = {610},
      cid          = {I:(DE-2719)1810002},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25655513},
      doi          = {10.1016/j.bbr.2015.01.040},
      url          = {https://pub.dzne.de/record/137854},
}