Morris water maze search strategy analysis in PDAPP mice before and after experimental traumatic brain injury

[1]  J. Pickard,et al.  Deficits in decision-making in head injury survivors. , 2005, Journal of neurotrauma.

[2]  T. Mcintosh,et al.  Motor and cognitive function evaluation following experimental traumatic brain injury , 2004, Neuroscience & Biobehavioral Reviews.

[3]  C. Janus Search strategies used by APP transgenic mice during navigation in the Morris water maze. , 2004, Learning & memory.

[4]  K. Hux,et al.  Accuracy, efficiency and preferences of survivors of traumatic brain injury when using three organization strategies to retrieve words , 2004, Brain injury.

[5]  Laura Petrosini,et al.  Automatic recognition of explorative strategies in the Morris water maze , 2003, Journal of Neuroscience Methods.

[6]  H. Lipp,et al.  Emotional instability but intact spatial cognition in adenosine receptor 1 knock out mice , 2003, Behavioural Brain Research.

[7]  D. Bennett,et al.  Alzheimer disease in the US population: prevalence estimates using the 2000 census. , 2003, Archives of neurology.

[8]  P. Colombo,et al.  Cognitive Strategy-Specific Increases in Phosphorylated cAMP Response Element-Binding Protein and c-Fos in the Hippocampus and Dorsal Striatum , 2003, The Journal of Neuroscience.

[9]  D. Cain,et al.  Combined β-Adrenergic and Cholinergic Antagonism Produces Behavioral and Cognitive Impairments in the Water Maze: Implications for Alzheimer Disease and Pharmacotherapy with β-Adrenergic Antagonists , 2003, Neuropsychopharmacology.

[10]  M. Kennedy,et al.  Predictions of recall and study strategy decisions after diffuse brain injury , 2003, Brain injury.

[11]  D. Holtzman,et al.  Apolipoprotein E4 Influences Amyloid Deposition But Not Cell Loss after Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease , 2002, The Journal of Neuroscience.

[12]  B. Hyman,et al.  Reversible Memory Loss in a Mouse Transgenic Model of Alzheimer's Disease , 2002, The Journal of Neuroscience.

[13]  Xin Wu,et al.  Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model , 2002, Nature Neuroscience.

[14]  S. Henriksen,et al.  Age-independent and age-related deficits in visuospatial learning, sleep–wake states, thermoregulation and motor activity in PDAPP mice , 2002, Brain Research.

[15]  E. R. Kloet,et al.  Reversal of cognitive deficit of apolipoprotein E knockout mice after repeated exposure to a common environmental experience , 2001, Neuroscience.

[16]  D. Diamond,et al.  Behavioral assessment of Alzheimer's transgenic mice following long-term Abeta vaccination: task specificity and correlations between Abeta deposition and spatial memory. , 2001, DNA and cell biology.

[17]  Guiquan Chen,et al.  A learning deficit related to age and β-amyloid plaques in a mouse model of Alzheimer's disease , 2000, Nature.

[18]  Hsiao-Wen Chen,et al.  Unusual spectral energy distribution of a galaxy previously reported to be at redshift 6.68 , 2000, Nature.

[19]  H. Lipp,et al.  Dissecting the Behaviour of Transgenic Mice: Is it the Mutation, the Genetic Background, or the Environment? , 2000, Experimental physiology.

[20]  J. Guralnik,et al.  Documented head injury in early adulthood and risk of Alzheimer’s disease and other dementias , 2000, Neurology.

[21]  J. Dodart,et al.  Behavioral deficits in APPV717F transgenic mice decient for the apolipoprotein E gene , 2000, Neuroreport.

[22]  K A Dunn,et al.  Traumatic brain injury in the United States: A public health perspective. , 1999, The Journal of head trauma rehabilitation.

[23]  H. Meziane,et al.  Behavioral disturbances in transgenic mice overexpressing the V717F beta-amyloid precursor protein. , 1999, Behavioral neuroscience.

[24]  J. Trojanowski,et al.  Brain trauma induces massive hippocampal neuron death linked to a surge in beta-amyloid levels in mice overexpressing mutant amyloid precursor protein. , 1998, The American journal of pathology.

[25]  J. Trojanowski,et al.  Twofold overexpression of human β‐amyloid precursor proteins in transgenic mice does not affect the neuromotor, cognitive, or neurodegenerative sequelae following experimental brain injury , 1998, The Journal of comparative neurology.

[26]  B. Hyman,et al.  Aβ Deposition Is Associated with Neuropil Changes, but not with Overt Neuronal Loss in the Human Amyloid Precursor Protein V717F (PDAPP) Transgenic Mouse , 1997, The Journal of Neuroscience.

[27]  D F Meaney,et al.  A model of parasagittal controlled cortical impact in the mouse: cognitive and histopathologic effects. , 1995, Journal of neurotrauma.

[28]  L. Mucke,et al.  Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein , 1995, Nature.

[29]  Ronald L. Hayes,et al.  A controlled cortical impact model of traumatic brain injury in the rat , 1991, Journal of Neuroscience Methods.

[30]  D. T. Yue,et al.  Calcium-sensitive inactivation in the gating of single calcium channels. , 1990, Science.

[31]  I. Whishaw Dissociating performance and learning deficits on spatial navigation tasks in rats subjected to cholinergic muscarinic blockade , 1989, Brain Research Bulletin.

[32]  R. Morris Synaptic plasticity and learning: selective impairment of learning rats and blockade of long-term potentiation in vivo by the N-methyl-D- aspartate receptor antagonist AP5 , 1989, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[33]  I. Whishaw,et al.  Cholinergic blockade in the rat impairs strategy selection but not learning and retention of nonspatial visual discrimination problems in a swimming pool. , 1988, Behavioral neuroscience.

[34]  Ian Q. Whishaw,et al.  Impairments in the acquisition, retention and selection of spatial navigation strategies after medial caudate-putamen lesions in rats , 1987, Behavioural Brain Research.

[35]  R. Morris Developments of a water-maze procedure for studying spatial learning in the rat , 1984, Journal of Neuroscience Methods.

[36]  R. Sutherland,et al.  Cholinergic receptor blockade impairs spatial localization by use of distal cues in the rat. , 1982, Journal of comparative and physiological psychology.

[37]  R. Morris,et al.  Place navigation impaired in rats with hippocampal lesions , 1982, Nature.

[38]  D. Cain,et al.  Combined beta-adrenergic and cholinergic antagonism produces behavioral and cognitive impairments in the water maze: implications for Alzheimer disease and pharmacotherapy with beta-adrenergic antagonists. , 2003, Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology.

[39]  J. Trojanowski,et al.  Traumatic brain injury in young, amyloid-beta peptide overexpressing transgenic mice induces marked ipsilateral hippocampal atrophy and diminished Abeta deposition during aging. , 1999, The Journal of comparative neurology.

[40]  E. Masliah,et al.  Neurodegenerative Alzheimer-like pathology in PDAPP 717V-->F transgenic mice. , 1998, Progress in brain research.

[41]  A. Heyman,et al.  Head trauma as a risk factor for Alzheimer's disease: a collaborative re-analysis of case-control studies. EURODEM Risk Factors Research Group. , 1991 .

[42]  G. Lynch,et al.  Selective impairment of learning and blockade of long-term potentiation by an N-methyl-D-aspartate receptor antagonist, AP5 , 1986, Nature.