Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice

[1]  T. Morgan,et al.  Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[2]  Alcino J. Silva,et al.  Autophosphorylation at Thr286 of the alpha calcium-calmodulin kinase II in LTP and learning. , 1998, Science.

[3]  E. Kandel,et al.  Genetic and Pharmacological Evidence for a Novel, Intermediate Phase of Long-Term Potentiation Suppressed by Calcineurin , 1998, Cell.

[4]  B. Hyman,et al.  Microglial response to amyloid plaques in APPsw transgenic mice. , 1998, The American journal of pathology.

[5]  J. Hardy,et al.  A new pathogenic mutation in the APP gene (I716V) increases the relative proportion of A beta 42(43). , 1997, Human molecular genetics.

[6]  B. Hyman,et al.  APPSW Transgenic Mice Develop Age‐related Aβ Deposits and Neuropil Abnormalities, but no Neuronal Loss in CA1 , 1997, Journal of neuropathology and experimental neurology.

[7]  J. Hardy,et al.  The presenilins and Alzheimer's disease. , 1997, Human molecular genetics.

[8]  E. Schuman,et al.  Neurotrophins and Time: Different Roles for TrkB Signaling in Hippocampal Long-Term Potentiation , 1997, Neuron.

[9]  Robert C. Malenka,et al.  Rab3A is essential for mossy fibre long-term potentiation in the hippocampus , 1997, Nature.

[10]  T. Bliss,et al.  Long-term potentiation in awake mutant mice , 1997, Nature.

[11]  M. Shapiro,et al.  Impaired learning and LTP in mice expressing the carboxy terminus of the Alzheimer amyloid precursor protein , 1997, Nature.

[12]  John Hardy,et al.  Amyloid, the presenilins and Alzheimer's disease , 1997, Trends in Neurosciences.

[13]  O. Steward,et al.  Genetic determinants of susceptibility to excitotoxic cell death: implications for gene targeting approaches. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[14]  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.

[15]  J. Hardy,et al.  Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 , 1996, Nature.

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

[17]  M. Dragunow A role for immediate-early transcription factors in learning and memory , 1996, Behavior genetics.

[18]  I. Nishimoto,et al.  Negative transactivation of cAMP response element by familial Alzheimer's mutants of APP. , 1996, The EMBO journal.

[19]  Thomas C. Südhof,et al.  The synaptic vesicle cycle: a cascade of protein–protein interactions , 1995, Nature.

[20]  A. Lüthi,et al.  Hippocampal long-term potentiation and neural cell adhesion molecules L1 and NCAM , 1994, Nature.

[21]  S. Younkin,et al.  An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants. , 1994, Science.

[22]  C. Finch Neuron atrophy during aging: programmed or sporadic? , 1993, Trends in Neurosciences.

[23]  S. Younkin,et al.  Release of excess amyloid beta protein from a mutant amyloid beta protein precursor. , 1993, Science.

[24]  T. Bliss,et al.  A synaptic model of memory: long-term potentiation in the hippocampus , 1993, Nature.

[25]  D. Selkoe,et al.  Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein production , 1992, Nature.

[26]  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.

[27]  D. Selkoe,et al.  Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increases beta-protein production. , 1992, Nature.

[28]  A. Hofman,et al.  Presenile dementia and cerebral haemorrhage linked to a mutation at codon 692 of the β–amyloid precursor protein gene , 1992, Nature Genetics.

[29]  S. J. Chen,et al.  Persistent protein kinase activation in the maintenance phase of long-term potentiation. , 1991, The Journal of biological chemistry.

[30]  J. Hardy,et al.  Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein gene , 1991, Nature.

[31]  B. Ghetti,et al.  A mutation in the amyloid precursor protein associated with hereditary Alzheimer's disease. , 1991, Science.

[32]  M. Pericak-Vance,et al.  Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease , 1991, Nature.

[33]  G. V. Van Hoesen,et al.  Perforant pathway changes and the memory impairment of Alzheimer's disease , 1986, Annals of neurology.