Spatial learning and exploration of environmental stimuli in 24-month-old female APP23 transgenic mice with the Swedish mutation

[1]  M. Staufenbiel,et al.  Neurobehavioral characterization of APP23 transgenic mice with the SHIRPA primary screen , 2005, Behavioural Brain Research.

[2]  J. Barnes,et al.  Ultrastructural and behavioural changes precede amyloid deposition in a transgenic model of Alzheimer’s disease , 2003, Neuroscience.

[3]  Jacob Raber,et al.  Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[4]  Robert Lalonde,et al.  Transgenic mice expressing the βAPP 695SWE mutation: effects on exploratory activity, anxiety, and motor coordination , 2003, Brain Research.

[5]  M. Staufenbiel,et al.  Regional brain cytochrome oxidase activity in β-amyloid precursor protein transgenic mice with the swedish mutation , 2003, Neuroscience.

[6]  D. Borchelt,et al.  Normal cognitive behavior in two distinct congenic lines of transgenic mice hyperexpressing mutant APPSWE , 2003, Neurobiology of Disease.

[7]  P. Kelly,et al.  Progressive age-related impairment of cognitive behavior in APP23 transgenic mice , 2003, Neurobiology of Aging.

[8]  R. D'Hooge,et al.  Age‐dependent cognitive decline in the APP23 model precedes amyloid deposition , 2003, The European journal of neuroscience.

[9]  M. Staufenbiel,et al.  Spatial learning, exploration, anxiety, and motor coordination in female APP23 transgenic mice with the Swedish mutation , 2002, Brain Research.

[10]  K. Bales,et al.  Behavioral impairment of APPV717F mice in fear conditioning: is it only cognition? , 2002, Behavioural Brain Research.

[11]  Markus Rudin,et al.  Compromised Hemodynamic Response in Amyloid Precursor Protein Transgenic Mice , 2002, The Journal of Neuroscience.

[12]  J. Sweatt,et al.  Accelerated Plaque Accumulation, Associative Learning Deficits, and Up-regulation of α7 Nicotinic Receptor Protein in Transgenic Mice Co-expressing Mutant Human Presenilin 1 and Amyloid Precursor Proteins* , 2002, The Journal of Biological Chemistry.

[13]  P. Kelly,et al.  Cholinergic Changes in the APP23 Transgenic Mouse Model of Cerebral Amyloidosis , 2002, The Journal of Neuroscience.

[14]  G. Arendash,et al.  Behavioral characterization of the Tg2576 transgenic model of Alzheimer's disease through 19 months , 2002, Physiology & Behavior.

[15]  George A. Carlson,et al.  The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's Disease , 2002, The Journal of Neuroscience.

[16]  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.

[17]  M. Staufenbiel,et al.  Amyloid-Associated Neuron Loss and Gliogenesis in the Neocortex of Amyloid Precursor Protein Transgenic Mice , 2002, The Journal of Neuroscience.

[18]  S. File,et al.  Factors controlling measures of anxiety and responses to novelty in the mouse , 2001, Behavioural Brain Research.

[19]  Lars Bertram,et al.  New Frontiers in Alzheimer's Disease Genetics , 2001, Neuron.

[20]  Yu-Min Kuo,et al.  The Evolution of Aβ Peptide Burden in the APP23 Transgenic Mice: Implications for Aβ Deposition in Alzheimer Disease , 2001, Molecular medicine.

[21]  S. Turner,et al.  Early-onset Amyloid Deposition and Cognitive Deficits in Transgenic Mice Expressing a Double Mutant Form of Amyloid Precursor Protein 695* , 2001, The Journal of Biological Chemistry.

[22]  F. Prato,et al.  A detailed ethological analysis of the mouse open field test: effects of diazepam, chlordiazepoxide and an extremely low frequency pulsed magnetic field , 2001, Neuroscience & Biobehavioral Reviews.

[23]  A. Holmes Targeted gene mutation approaches to the study of anxiety-like behavior in mice , 2001, Neuroscience & Biobehavioral Reviews.

[24]  M. Staufenbiel,et al.  Spontaneous Hemorrhagic Stroke in a Mouse Model of Cerebral Amyloid Angiopathy , 2001, The Journal of Neuroscience.

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

[26]  Ralph A. Nixon,et al.  Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease , 2000, Nature.

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

[28]  J. Cummings,et al.  Neurobehavioral and neuropsychiatric symptoms in Alzheimer's disease: characteristics and treatment. , 2000, Neurologic clinics.

[29]  F. Leuven,et al.  Single and multiple transgenic mice as models for Alzheimer’s disease , 2000, Progress in Neurobiology.

[30]  B. Sommer,et al.  Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

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

[32]  M. Frotscher,et al.  Cerebral Amyloid Induces Aberrant Axonal Sprouting and Ectopic Terminal Formation in Amyloid Precursor Protein Transgenic Mice , 1999, The Journal of Neuroscience.

[33]  B. Sommer,et al.  Association of microglia with amyloid plaques in brains of APP23 transgenic mice. , 1999, The American journal of pathology.

[34]  K. Duff,et al.  Behavioral Changes in Transgenic Mice Expressing Both Amyloid Precursor Protein and Presenilin-1 Mutations: Lack of Association with Amyloid Deposits , 1999, Behavior genetics.

[35]  Veerle Baekelandt,et al.  Early Phenotypic Changes in Transgenic Mice That Overexpress Different Mutants of Amyloid Precursor Protein in Brain* , 1999, The Journal of Biological Chemistry.

[36]  T. Bliss,et al.  Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice , 1999, Nature Neuroscience.

[37]  G. Frisoni,et al.  Behavioral Syndromes in Alzheimer’s Disease: Description and Correlates , 1999, Dementia and Geriatric Cognitive Disorders.

[38]  B. Sommer,et al.  Neuron loss in APP transgenic mice , 1998, Nature.

[39]  B. Sommer,et al.  Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[40]  D. Borchelt,et al.  Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins , 1997, Neuron.

[41]  Allan I. Levey,et al.  Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo , 1996, Neuron.

[42]  S. Younkin,et al.  Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.

[43]  S. Weintraub Four neuropsychological profiles in dementia , 1996 .

[44]  R. Holson,et al.  Mesial prefrontal cortical lesions and timidity in rats. I. Reactivity to aversive stimuli , 1986, Physiology & Behavior.

[45]  S. File,et al.  Validation of open : closed arm entries in an elevated plus-maze as a measure of anxiety in the rat , 1985, Journal of Neuroscience Methods.

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

[47]  W. N. Dember,et al.  Spontaneous alteration after free and forced trials. , 1959, Canadian journal of psychology.

[48]  J. Hardy,et al.  Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes , 1998, Nature Medicine.