Increased exploratory activity of APP23 mice in a novel environment is reversed by siRNA

[1]  Davide Viggiano,et al.  The hyperactive syndrome: Metanalysis of genetic alterations, pharmacological treatments and brain lesions which increase locomotor activity , 2008, Behavioural Brain Research.

[2]  M. Staufenbiel,et al.  Altered ingestive behavior, weight changes, and intact olfactory sense in an APP overexpression model. , 2008, Behavioral neuroscience.

[3]  S. Itohara,et al.  Cortical Glutamatergic Neurons Mediate the Motor Sedative Action of Diazepam , 2008, Molecular Pharmacology.

[4]  P. Kelly,et al.  Amyloid precursor protein knockout mice show age-dependent deficits in passive avoidance learning , 2008, Behavioural Brain Research.

[5]  P. Kelly,et al.  Amyloid precursor protein knockdown by siRNA impairs spontaneous alternation in adult mice , 2007, Journal of neurochemistry.

[6]  Roger M. Nitsch,et al.  Intracellular Aβ and cognitive deficits precede β-amyloid deposition in transgenic arcAβ mice , 2007, Neurobiology of Aging.

[7]  M. Staufenbiel,et al.  Selective vulnerability of different types of commissural neurons for amyloid beta-protein-induced neurodegeneration in APP23 mice correlates with dendritic tree morphology. , 2006, Brain : a journal of neurology.

[8]  Y. Larmet,et al.  Unraveling in vivo Functions of Amyloid Precursor Protein: Insights from Knockout and Knockdown Studies , 2006, Neurodegenerative Diseases.

[9]  J. Glowinski,et al.  Behavioral sensitization to amphetamine results from an uncoupling between noradrenergic and serotonergic neurons. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[10]  J. Girault,et al.  Plasticity-Associated Gene Krox24/Zif268 Is Required for Long-Lasting Behavioral Effects of Cocaine , 2006, The Journal of Neuroscience.

[11]  Z. Zuo,et al.  Allele-specific silencing of Alzheimer's disease genes: the amyloid precursor protein genes with Swedish or London mutations. , 2006, Gene.

[12]  Mark Bowlby,et al.  Early-onset behavioral and synaptic deficits in a mouse model of Alzheimer's disease. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[13]  M. Gallagher,et al.  A specific amyloid-β protein assembly in the brain impairs memory , 2006, Nature.

[14]  H. Paulson,et al.  Allele-specific RNA interference for neurological disease , 2006, Gene Therapy.

[15]  M. Ohno,et al.  Temporal memory deficits in Alzheimer's mouse models: rescue by genetic deletion of BACE1 , 2006, The European journal of neuroscience.

[16]  Inder M Verma,et al.  Targeting BACE1 with siRNAs ameliorates Alzheimer disease neuropathology in a transgenic model , 2005, Nature Neuroscience.

[17]  Dieter Huesken,et al.  Design of a genome-wide siRNA library using an artificial neural network , 2005, Nature Biotechnology.

[18]  R. Morris,et al.  Conditional Inactivation of Presenilin 1 Prevents Amyloid Accumulation and Temporarily Rescues Contextual and Spatial Working Memory Impairments in Amyloid Precursor Protein Transgenic Mice , 2005, The Journal of Neuroscience.

[19]  D. Holtzman,et al.  Treatment with an Amyloid-β Antibody Ameliorates Plaque Load, Learning Deficits, and Hippocampal Long-Term Potentiation in a Mouse Model of Alzheimer's Disease , 2005, The Journal of Neuroscience.

[20]  G. Higgins,et al.  Age-progressing cognitive impairments and neuropathology in transgenic CRND8 mice , 2005, Behavioural Brain Research.

[21]  D. Borchelt,et al.  Environmental Enrichment Mitigates Cognitive Deficits in a Mouse Model of Alzheimer's Disease , 2005, The Journal of Neuroscience.

[22]  P. Deyn,et al.  Analysis of cholinergic markers, biogenic amines, and amino acids in the CNS of two APP overexpression mouse models , 2005, Neurochemistry International.

[23]  Kefei Chen,et al.  Behavioral phenotypes of amyloid‐based genetically modified mouse models of Alzheimer's disease , 2005, Genes, brain, and behavior.

[24]  R. Tanzi,et al.  Twenty Years of the Alzheimer’s Disease Amyloid Hypothesis: A Genetic Perspective , 2005, Cell.

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

[26]  F. Natt,et al.  Neurochemical and behavioral consequences of widespread gene knockdown in the adult mouse brain by using nonviral RNA interference. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[27]  S. Engelborghs,et al.  Altered circadian locomotor activity in APP23 mice: a model for BPSD disturbances , 2004, The European journal of neuroscience.

[28]  M. Staufenbiel,et al.  Spatial learning and exploration of environmental stimuli in 24-month-old female APP23 transgenic mice with the Swedish mutation , 2004, Brain Research.

[29]  F. Natt,et al.  siRNA relieves chronic neuropathic pain. , 2004, Nucleic acids research.

[30]  H. Paulson,et al.  Targeting Alzheimer's disease genes with RNA interference: an efficient strategy for silencing mutant alleles. , 2004, Nucleic acids research.

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

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

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

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

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

[36]  G. Arendash,et al.  Intra- and intertask relationships in a behavioral test battery given to Tg2576 transgenic mice and controls , 2002, Physiology & Behavior.

[37]  T. Sotnikova,et al.  Hyperactivity, elevated dopaminergic transmission, and response to amphetamine in M1 muscarinic acetylcholine receptor-deficient mice , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[38]  J. Bureš,et al.  Specific spatial learning deficits become severe with age in β-amyloid precursor protein transgenic mice that harbor diffuse β-amyloid deposits but do not form plaques , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[39]  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.

[40]  J. Wess,et al.  Hyperactivity and Intact Hippocampus-Dependent Learning in Mice Lacking the M1 Muscarinic Acetylcholine Receptor , 2001, The Journal of Neuroscience.

[41]  D. Selkoe.  Alzheimer's disease: genes, proteins, and therapy. , 2001, Physiological reviews.

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

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

[44]  J. Hardy,et al.  Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease , 2000, Nature.

[45]  M. Staufenbiel,et al.  Pathogenic Mechanisms of Alzheimer's Disease Analyzed in the APP23 Transgenic Mouse Model , 2000, Annals of the New York Academy of Sciences.

[46]  W. Banks,et al.  Site-directed antisense oligonucleotide decreases the expression of amyloid precursor protein and reverses deficits in learning and memory in aged SAMP8 mice , 2000, Peptides.

[47]  R. Gainetdinov,et al.  Muscarinic Supersensitivity and Impaired Receptor Desensitization in G Protein–Coupled Receptor Kinase 5–Deficient Mice , 1999, Neuron.

[48]  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.

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

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

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

[52]  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.

[53]  S. Cabib,et al.  PSYCHOPHARMACOLOGY OF DOPAMINE: THE CONTRIBUTION OF COMPARATIVE STUDIES IN INBRED STRAINS OF MICE , 1997, Progress in Neurobiology.

[54]  P. Paganetti,et al.  Effect of alkalizing agents on the processing of the β-amyloid precursor protein , 1996, Brain Research.

[55]  G. Dawson,et al.  β-amyloid precursor protein-deficient mice show reactive gliosis and decreased locomotor activity , 1995, Cell.

[56]  Thomas Rülicke,et al.  Behavioral and anatomical deficits in mice homozygous for a modified β-amyloid precursor protein gene , 1994, Cell.

[57]  I. Whishaw,et al.  Disruption of central cholinergic systems in the rat by basal forebrain lesions or atropine: Effects on feeding, sensorimotor behaviour, locomotor activity and spatial navigation , 1985, Behavioural Brain Research.

[58]  R. Nitsch,et al.  Intracellular Abeta and cognitive deficits precede beta-amyloid deposition in transgenic arcAbeta mice. , 2007, Neurobiology of aging.

[59]  D. Holtzman,et al.  Treatment with an amyloid-beta antibody ameliorates plaque load, learning deficits, and hippocampal long-term potentiation in a mouse model of Alzheimer's disease. , 2005, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[60]  J. Hardy,et al.  A beta peptide vaccination prevents memory loss in an animal model of Alzheimer's disease. , 2000, Nature.

[61]  P. S. St George-Hyslop,et al.  A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease. , 2000, Nature.

[62]  Y. Lamberty,et al.  Cholinergic modulation of spatial learning in mice in a Morris-type water maze. , 1991, Archives internationales de pharmacodynamie et de therapie.