Time-course of glial changes in the hyperhomocysteinemia model of vascular cognitive impairment and dementia (VCID)

[1]  O. Ottersen,et al.  Mechanisms underlying AQP4 accumulation in astrocyte endfeet , 2015, Glia.

[2]  Y. Qian,et al.  IL-17A is implicated in lipopolysaccharide-induced neuroinflammation and cognitive impairment in aged rats via microglial activation , 2015, Journal of Neuroinflammation.

[3]  J. Schneider,et al.  Vascular contributions to cognitive impairment and dementia including Alzheimer's disease , 2015, Alzheimer's & Dementia.

[4]  J. Guzowski,et al.  Systemic lipopolysaccharide administration impairs retrieval of context–object discrimination, but not spatial, memory: Evidence for selective disruption of specific hippocampus-dependent memory functions during acute neuroinflammation , 2015, Brain, Behavior, and Immunity.

[5]  N. MacAulay,et al.  Kir4.1-mediated spatial buffering of K+: Experimental challenges in determination of its temporal and quantitative contribution to K+ clearance in the brain , 2014, Channels.

[6]  M. Yasui,et al.  Sustained Down-regulation of β-Dystroglycan and Associated Dysfunctions of Astrocytic Endfeet in Epileptic Cerebral Cortex* , 2014, The Journal of Biological Chemistry.

[7]  Alyssa A. Gamaldo,et al.  Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis , 2014, BMC Public Health.

[8]  D. Wilcock,et al.  β-amyloid deposition is shifted to the vasculature and memory impairment is exacerbated when hyperhomocysteinemia is induced in APP/PS1 transgenic mice , 2014, Alzheimer's Research & Therapy.

[9]  George Em Karniadakis,et al.  Potassium buffering in the neurovascular unit: models and sensitivity analysis. , 2013, Biophysical journal.

[10]  Charles D. Smith,et al.  Induction of Hyperhomocysteinemia Models Vascular Dementia by Induction of Cerebral Microhemorrhages and Neuroinflammation , 2013, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[11]  A. Butt,et al.  Relationship between glial potassium regulation and axon excitability: A role for glial Kir4.1 channels , 2012, Glia.

[12]  Arne Klungland,et al.  Evidence that compromised K+ spatial buffering contributes to the epileptogenic effect of mutations in the human kir4.1 gene (KCNJ10) , 2011, Glia.

[13]  Tim David,et al.  Models of neurovascular coupling via potassium and EET signalling. , 2011, Journal of theoretical biology.

[14]  U. Heinemann,et al.  Impact of aquaporin‐4 channels on K+ buffering and gap junction coupling in the hippocampus , 2011, Glia.

[15]  Aaron M. Beedle,et al.  Evidence for a role of dystroglycan regulating the membrane architecture of astroglial endfeet , 2011, The European journal of neuroscience.

[16]  K. Langa,et al.  Vascular Cognitive Impairment: Disease Mechanisms and Therapeutic Implications , 2011, Neurotherapeutics.

[17]  R. Bischoff,et al.  Physiology and pathophysiology of matrix metalloproteases , 2010, Amino Acids.

[18]  M. Nelson,et al.  Potassium channels and neurovascular coupling. , 2010, Circulation journal : official journal of the Japanese Circulation Society.

[19]  T. Iftner,et al.  p38γ MAPK Cooperates with c-Jun in trans-Activating Matrix Metalloproteinase 9* , 2010, The Journal of Biological Chemistry.

[20]  C. Colton,et al.  Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer's disease , 2009, Neuroscience.

[21]  B. Shukitt-Hale,et al.  B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice , 2008, Proceedings of the National Academy of Sciences.

[22]  Nastaran Gharkholonarehe,et al.  Progression of Amyloid Pathology to Alzheimer's Disease Pathology in an Amyloid Precursor Protein Transgenic Mouse Model by Removal of Nitric Oxide Synthase 2 , 2008, The Journal of Neuroscience.

[23]  L. Kaczmarek,et al.  β-Dystroglycan as a Target for MMP-9, in Response to Enhanced Neuronal Activity* , 2007, Journal of Biological Chemistry.

[24]  Eric A Newman,et al.  Neurovascular Coupling Is Not Mediated by Potassium Siphoning from Glial Cells , 2007, The Journal of Neuroscience.

[25]  T. Klockgether,et al.  Long-term cognitive impairment, neuronal loss and reduced cortical cholinergic innervation after recovery from sepsis in a rodent model , 2007, Experimental Neurology.

[26]  D. Diamond,et al.  Two-day radial-arm water maze learning and memory task; robust resolution of amyloid-related memory deficits in transgenic mice , 2006, Nature Protocols.

[27]  D. Holtzman,et al.  Matrix Metalloproteinases Expressed by Astrocytes Mediate Extracellular Amyloid-β Peptide Catabolism , 2006, The Journal of Neuroscience.

[28]  U. Heinemann,et al.  The Impact of Astrocytic Gap Junctional Coupling on Potassium Buffering in the Hippocampus , 2006, The Journal of Neuroscience.

[29]  S. Chakrabarti,et al.  Regulation of matrix metalloproteinase‐9 (MMP‐9) in TNF‐stimulated neutrophils: novel pathways for tertiary granule release , 2006, Journal of leukocyte biology.

[30]  A. Butt,et al.  Inwardly rectifying potassium channels (Kir) in central nervous system glia: a special role for Kir4.1 in glial functions , 2006, Journal of cellular and molecular medicine.

[31]  O. P. Ottersen,et al.  Anchoring of aquaporin-4 in brain: Molecular mechanisms and implications for the physiology and pathophysiology of water transport , 2004, Neuroscience.

[32]  M. Simard,et al.  The neurobiology of glia in the context of water and ion homeostasis , 2004, Neuroscience.

[33]  K. Langa,et al.  Mixed dementia: emerging concepts and therapeutic implications. , 2004, JAMA.

[34]  D. Wilcock,et al.  Passive immunotherapy against Aβ in aged APP-transgenic mice reverses cognitive deficits and depletes parenchymal amyloid deposits in spite of increased vascular amyloid and microhemorrhage , 2004, Journal of Neuroinflammation.

[35]  Susumu Mori,et al.  Alpha syntrophin deletion removes the perivascular but not the endothelial pool of aquaporin‐4 at the blood‐brain barrier and delays the development of brain edema in an experimental model of acute hyponatremia , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[36]  Ole Petter Ottersen,et al.  An α-syntrophin-dependent pool of AQP4 in astroglial end-feet confers bidirectional water flow between blood and brain , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[37]  Mark Ellisman,et al.  Distribution of rSlo Ca2+-activated K+ channels in rat astrocyte perivascular endfeet , 2002, Brain Research.

[38]  P. Kofuji,et al.  Dystrophin Dp71 Is Critical for the Clustered Localization of Potassium Channels in Retinal Glial Cells , 2002, The Journal of Neuroscience.

[39]  Thomas D. Schmittgen,et al.  Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.

[40]  C. Bouras,et al.  Immediate causes of death of demented and non‐demented elderly , 2000, Acta neurologica Scandinavica. Supplementum.

[41]  R Clarke,et al.  Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. , 1998, Archives of neurology.

[42]  V. Hachinski,et al.  Fallacies in the pathological confirmation of the diagnosis of Alzheimer’s disease , 1998, Journal of neurology, neurosurgery, and psychiatry.

[43]  S. Vollset,et al.  Homocysteine and cardiovascular disease. , 1998, Annual review of medicine.

[44]  E. Newman,et al.  Control of extracellular potassium levels by retinal glial cell K+ siphoning. , 1984, Science.