Amyloid-β–induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks
暂无分享,去创建一个
[1] D. Selkoe. Alzheimer's disease. , 2011, Cold Spring Harbor perspectives in biology.
[2] Rie Teraoka,et al. A Mouse Model of Amyloid β Oligomers: Their Contribution to Synaptic Alteration, Abnormal Tau Phosphorylation, Glial Activation, and Neuronal Loss In Vivo , 2010, The Journal of Neuroscience.
[3] James B Leverenz,et al. Alzheimer's disease phenotypes and genotypes associated with mutations in presenilin 2. , 2010, Brain : a journal of neurology.
[4] Roberto Malinow,et al. Amyloid beta from axons and dendrites reduces local spine number and plasticity , 2010, Nature Neuroscience.
[5] Hui Zheng,et al. Amyloid Precursor Protein Regulates Cav1.2 L-type Calcium Channel Levels and Function to Influence GABAergic Short-Term Plasticity , 2009, The Journal of Neuroscience.
[6] R. Mahley,et al. GABAergic interneuron dysfunction impairs hippocampal neurogenesis in adult apolipoprotein E4 knockin mice. , 2009, Cell stem cell.
[7] I. Slutsky,et al. Amyloid-β as a positive endogenous regulator of release probability at hippocampal synapses , 2009, Nature Neuroscience.
[8] K. Herrup. Faculty Opinions recommendation of Divergent pathways mediate spine alterations and cell death induced by amyloid-beta, wild-type tau, and R406W tau. , 2009 .
[9] R. Brandt,et al. Divergent Pathways Mediate Spine Alterations and Cell Death Induced by Amyloid-β, Wild-Type Tau, and R406W Tau , 2009, The Journal of Neuroscience.
[10] Seiji Nishino,et al. Amyloid-β Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle , 2009, Science.
[11] O. Arancio,et al. MAPK, β-amyloid and synaptic dysfunction: the role of RAGE , 2009, Expert review of neurotherapeutics.
[12] Keith A. Johnson,et al. Amyloid Deposition Is Associated with Impaired Default Network Function in Older Persons without Dementia , 2009, Neuron.
[13] Shaomin Li,et al. Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate Uptake , 2009, Neuron.
[14] G. Zamponi. Faculty Opinions recommendation of Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers. , 2009 .
[15] L. Mucke,et al. Epilepsy and cognitive impairments in Alzheimer disease. , 2009, Archives of neurology.
[16] Sylvain Rheims,et al. Amyloid β-Induced Neuronal Hyperexcitability Triggers Progressive Epilepsy , 2009, The Journal of Neuroscience.
[17] B. Hyman,et al. Synchronous Hyperactivity and Intercellular Calcium Waves in Astrocytes in Alzheimer Mice , 2009, Science.
[18] John W. Gilbert,et al. Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-β Oligomers , 2009, Nature.
[19] R. Kayed,et al. Annular Protofibrils Are a Structurally and Functionally Distinct Type of Amyloid Oligomer* , 2009, Journal of Biological Chemistry.
[20] A. Palmeri,et al. Picomolar Amyloid-β Positively Modulates Synaptic Plasticity and Memory in Hippocampus , 2008, The Journal of Neuroscience.
[21] C. Glabe,et al. Structural Classification of Toxic Amyloid Oligomers* , 2008, Journal of Biological Chemistry.
[22] R. Tanzi,et al. Thirty years of Alzheimer's disease genetics: the implications of systematic meta-analyses , 2008, Nature Reviews Neuroscience.
[23] Arthur Konnerth,et al. Clusters of Hyperactive Neurons Near Amyloid Plaques in a Mouse Model of Alzheimer's Disease , 2008, Science.
[24] D. Selkoe,et al. Soluble oligomers of the amyloid β-protein impair synaptic plasticity and behavior , 2008, Behavioural Brain Research.
[25] L. Mucke,et al. Enkephalin Elevations Contribute to Neuronal and Behavioral Impairments in a Transgenic Mouse Model of Alzheimer's Disease , 2008, The Journal of Neuroscience.
[26] J. McNamara,et al. Does Epileptiform Activity Contribute to Cognitive Impairment in Alzheimer's Disease? , 2007, Neuron.
[27] Anatol C. Kreitzer,et al. Aberrant Excitatory Neuronal Activity and Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer's Disease , 2007, Neuron.
[28] D. Kullmann,et al. Long-term synaptic plasticity in hippocampal interneurons , 2007, Nature Reviews Neuroscience.
[29] G. Perea,et al. Astrocytes Potentiate Transmitter Release at Single Hippocampal Synapses , 2007, Science.
[30] L. Mucke,et al. Accelerating Amyloid-β Fibrillization Reduces Oligomer Levels and Functional Deficits in Alzheimer Disease Mouse Models* , 2007, Journal of Biological Chemistry.
[31] D. Selkoe,et al. Aβ Oligomers – a decade of discovery , 2007, Journal of neurochemistry.
[32] L. Mucke,et al. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.
[33] Bernardo L Sabatini,et al. Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway , 2007, The Journal of Neuroscience.
[34] Kiralee M. Hayashi,et al. The topography of grey matter involvement in early and late onset Alzheimer's disease. , 2007, Brain : a journal of neurology.
[35] Istvan Mody,et al. Seizures and enhanced cortical GABAergic inhibition in two mouse models of human autosomal dominant nocturnal frontal lobe epilepsy , 2006, Proceedings of the National Academy of Sciences.
[36] R. Malinow,et al. AMPAR Removal Underlies Aβ-Induced Synaptic Depression and Dendritic Spine Loss , 2006, Neuron.
[37] Florence Pasquier,et al. Phenotype associated with APP duplication in five families. , 2006, Brain : a journal of neurology.
[38] L. Mucke,et al. A network dysfunction perspective on neurodegenerative diseases , 2006, Nature.
[39] Yaakov Stern,et al. Incidence and Predictors of Seizures in Patients with Alzheimer's Disease , 2006, Epilepsia.
[40] R. Mahley,et al. Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[41] M. Gallagher,et al. A specific amyloid-β protein assembly in the brain impairs memory , 2006, Nature.
[42] M. Doran,et al. Clinical phenotypic heterogeneity of Alzheimer's disease associated with mutations of the presenilin–1 gene , 2006, Journal of Neurology.
[43] Steven Mennerick,et al. Synaptic Activity Regulates Interstitial Fluid Amyloid-β Levels In Vivo , 2005, Neuron.
[44] H. Cai,et al. BACE1, a Major Determinant of Selective Vulnerability of the Brain to Amyloid-β Amyloidogenesis, is Essential for Cognitive, Emotional, and Synaptic Functions , 2005, The Journal of Neuroscience.
[45] J. Morris,et al. Novel presenilin 1 mutation (S170F) causing Alzheimer disease with Lewy bodies in the third decade of life. , 2005, Archives of neurology.
[46] A. Vezzani,et al. Brain Inflammation in Epilepsy: Experimental and Clinical Evidence , 2005, Epilepsia.
[47] L. Mucke,et al. Fyn Kinase Induces Synaptic and Cognitive Impairments in a Transgenic Mouse Model of Alzheimer's Disease , 2005, The Journal of Neuroscience.
[48] Bertrand Z. Yeung,et al. Vulnerability of Dentate Granule Cells to Disruption of Arc Expression in Human Amyloid Precursor Protein Transgenic Mice , 2005, The Journal of Neuroscience.
[49] Benjamin J. Shannon,et al. Molecular, Structural, and Functional Characterization of Alzheimer's Disease: Evidence for a Relationship between Default Activity, Amyloid, and Memory , 2005, The Journal of Neuroscience.
[50] P. Greengard,et al. Regulation of NMDA receptor trafficking by amyloid-β , 2005, Nature Neuroscience.
[51] R. Tanzi,et al. Twenty Years of the Alzheimer’s Disease Amyloid Hypothesis: A Genetic Perspective , 2005, Cell.
[52] M. Staufenbiel,et al. Neurobehavioral characterization of APP23 transgenic mice with the SHIRPA primary screen , 2005, Behavioural Brain Research.
[53] S. Gobbo,et al. Neuronal Synchrony Mediated by Astrocytic Glutamate through Activation of Extrasynaptic NMDA Receptors , 2005, Neuron.
[54] D. Selkoe,et al. Natural oligomers of the amyloid-β protein specifically disrupt cognitive function , 2005, Nature Neuroscience.
[55] S. Gobbo,et al. Neuronal Synchrony Mediated by Astrocytic Glutamate through Activation of Extrasynaptic NMDA Receptors , 2004, Neuron.
[56] J. Votaw,et al. The role of positron emission tomography with [18F]fluorodeoxyglucose in the evaluation of the epilepsies. , 2004, Neuroimaging clinics of North America.
[57] M. Sheng,et al. Role of NMDA Receptor Subtypes in Governing the Direction of Hippocampal Synaptic Plasticity , 2004, Science.
[58] E. Kandel,et al. Loss of Presenilin Function Causes Impairments of Memory and Synaptic Plasticity Followed by Age-Dependent Neurodegeneration , 2004, Neuron.
[59] R. Anwyl,et al. Block of Long-Term Potentiation by Naturally Secreted and Synthetic Amyloid β-Peptide in Hippocampal Slices Is Mediated via Activation of the Kinases c-Jun N-Terminal Kinase, Cyclin-Dependent Kinase 5, and p38 Mitogen-Activated Protein Kinase as well as Metabotropic Glutamate Receptor Type 5 , 2004, The Journal of Neuroscience.
[60] Laurie A. Miller,et al. Senile plaques in temporal lobe epilepsy , 1994, Acta Neuropathologica.
[61] 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.
[62] R. Malinow,et al. APP Processing and Synaptic Function , 2003, Neuron.
[63] J. Hardy,et al. The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .
[64] J. David Sweatt,et al. β-Amyloid Peptide Activates α7 Nicotinic Acetylcholine Receptors Expressed in Xenopus Oocytes* , 2002, The Journal of Biological Chemistry.
[65] W. K. Cullen,et al. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.
[66] N. Danbolt. Glutamate uptake , 2001, Progress in Neurobiology.
[67] C. Finch,et al. Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum? , 2001, Trends in Neurosciences.
[68] R. Anwyl,et al. Use-Dependent Effects of Amyloidogenic Fragments of β-Amyloid Precursor Protein on Synaptic Plasticity in Rat Hippocampus In Vivo , 2001, The Journal of Neuroscience.
[69] Hai Lin,et al. Fresh and nonfibrillar amyloid β protein(1–40) induces rapid cellular degeneration in aged human fibroblasts: evidence for AβP‐channel‐mediated cellular toxicity , 2000, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[70] Kang Hu,et al. High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation , 2000, The Journal of Neuroscience.
[71] C. Broeckhoven,et al. Behavioral Disturbances without Amyloid Deposits in Mice Overexpressing Human Amyloid Precursor Protein with Flemish (A692G) or Dutch (E693Q) Mutation , 2000, Neurobiology of Disease.
[72] R. Nicoll,et al. Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[73] G. Collingridge,et al. Mechanisms contributing to the deficits in hippocampal synaptic plasticity in mice lacking amyloid precursor protein , 1999, Neuropharmacology.
[74] T. Bliss,et al. Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice , 1999, Nature Neuroscience.
[75] J. Haines,et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium. , 1997, JAMA.
[76] J. Haines,et al. Effects of Age, Sex, and Ethnicity on the Association Between Apolipoprotein E Genotype and Alzheimer Disease: A Meta-analysis , 1997 .
[77] N. Foster,et al. Metabolic reduction in the posterior cingulate cortex in very early Alzheimer's disease , 1997, Annals of neurology.
[78] D. Salmon,et al. Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment , 1991, Annals of neurology.
[79] S. DeKosky,et al. Synapse loss in frontal cortex biopsies in Alzheimer's disease: Correlation with cognitive severity , 1990, Annals of neurology.
[80] R. S. Williams,et al. A prospective study of Alzheimer disease in Down syndrome. , 1989, Archives of neurology.
[81] A. Baer. The genetic perspective , 1977 .