Spatial learning, exploration, anxiety, and motor coordination in female APP23 transgenic mice with the Swedish mutation

[1]  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.

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

[3]  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.

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

[5]  D. Diamond,et al.  Progressive, age-related behavioral impairments in transgenic mice carrying both mutant amyloid precursor protein and presenilin-1 transgenes , 2001, Brain Research.

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

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

[8]  S. Paul,et al.  Neuroanatomical Abnormalities in Behaviorally Characterized APPV717F Transgenic Mice , 2000, Neurobiology of Disease.

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

[10]  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.

[11]  D. Selkoe,et al.  Translating cell biology into therapeutic advances in Alzheimer's disease , 1999, Nature.

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

[13]  Robert Lalonde,et al.  Motor coordination and spatial orientation are affected by neurofilament maldistribution: correlations with regional brain activity of cytochrome oxidase , 1999, Experimental Brain Research.

[14]  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.

[15]  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.

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

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

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

[19]  C. Jack,et al.  Rate of medial temporal lobe atrophy in typical aging and Alzheimer's disease , 1998, Neurology.

[20]  C. Goetz,et al.  5-Hydroxytryptophan-induced myoclonus in guinea pigs: mediation through 5-HT1/2 receptor subtypes. , 1998, European journal of pharmacology.

[21]  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.

[22]  R. D'Hooge,et al.  Spatial learning deficit in mice expressing human 751-amino acid beta-amyloid precursor protein. , 1996, Neuroreport.

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

[24]  D. Premkumar,et al.  Molecular aspects of inflammatory and immune responses in Alzheimer's disease , 1996, Neurobiology of Aging.

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

[26]  D. Borchelt,et al.  Age-related CNS disorder and early death in transgenic FVB/N mice overexpressing Alzheimer amyloid precursor proteins , 1995, Neuron.

[27]  T. Iwatsubo,et al.  Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43) , 1994, Neuron.

[28]  B. Winblad,et al.  A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N–terminus of β–amyloid , 1992, Nature Genetics.

[29]  J. Ulrich,et al.  Alzheimer's Disease: A Description of the Structural Lesions , 1991, Brain pathology.

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

[31]  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.

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

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

[34]  Robert Lalonde,et al.  Chapter 4.3 Motor performance of spontaneous murine mutations with cerebellar atrophy , 1999 .

[35]  H. Wiśniewski,et al.  Morphology of the aging brain, human and animal. , 1973, Progress in brain research.