Pathological reorganization of NMDA receptors subunits and postsynaptic protein PSD-95 distribution in Alzheimer's disease.
暂无分享,去创建一个
Eric Tardif | G. Leuba | R. Kraftsik | E. Tardif | B. Riederer | A. Savioz | Armand Savioz | Beat Michel Riederer | Rudolf Kraftsik | Genevieve Leuba | Andre Vernay | A. Vernay
[1] C. Cotman,et al. Density and distribution of NMDA receptors in the human hippocampus in Alzheimer's disease , 1986, Brain Research.
[2] G. Knott,et al. PSD-95 promotes synaptogenesis and multiinnervated spine formation through nitric oxide signaling , 2008, The Journal of cell biology.
[3] W. Klein,et al. Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease , 2007, The Journal of Neuroscience.
[4] T. Sacktor,et al. Postsynaptic degeneration as revealed by PSD-95 reduction occurs after advanced Aβ and tau pathology in transgenic mouse models of Alzheimer’s disease , 2011, Acta Neuropathologica.
[5] M. Bear,et al. Ubiquitination Regulates PSD-95 Degradation and AMPA Receptor Surface Expression , 2003, Neuron.
[6] Suneil K. Kalia,et al. NMDA receptors in clinical neurology: excitatory times ahead , 2008, The Lancet Neurology.
[7] D. Bennett,et al. Decreases in soluble α-synuclein in frontal cortex correlate with cognitive decline in the elderly , 2004, Neuroscience Letters.
[8] P. Greengard,et al. Regulation of NMDA receptor trafficking by amyloid-β , 2005, Nature Neuroscience.
[9] E. Masliah,et al. Alterations in glutamate receptor 2/3 subunits and amyloid precursor protein expression during the course of Alzheimer’s disease and Lewy body variant , 1997, Acta Neuropathologica.
[10] A. El-Husseini,et al. Excitation Control: Balancing PSD-95 Function at the Synapse , 2008, Frontiers in molecular neuroscience.
[11] X. Zhao,et al. The effects of aging on N-methyl-d-aspartate receptor subunits in the synaptic membrane and relationships to long-term spatial memory , 2009, Neuroscience.
[12] D. Pei,et al. NR2B-Containing NMDA Receptors Expression and Their Relationship to Apoptosis in Hippocampus of Alzheimer’s Disease-Like Rats , 2012, Neurochemical Research.
[13] Vishnu Suppiramaniam,et al. Amyloid beta peptides and glutamatergic synaptic dysregulation , 2008, Experimental Neurology.
[14] M. Sheng,et al. Synaptic Accumulation of PSD-95 and Synaptic Function Regulated by Phosphorylation of Serine-295 of PSD-95 , 2007, Neuron.
[15] Roger A. Nicoll,et al. Rapid Bidirectional Switching of Synaptic NMDA Receptors , 2007, Neuron.
[16] Masahiko Watanabe,et al. PSD-95 Uncouples Dopamine–Glutamate Interaction in the D1/PSD-95/NMDA Receptor Complex , 2009, The Journal of Neuroscience.
[17] R. Wenthold,et al. Distribution of Glutamate Receptor Subunit NMDAR1 in the Hippocampus of Normal Elderly and Patients with Alzheimer's Disease , 1999, Experimental Neurology.
[18] R. Malenka,et al. Destabilization of the Postsynaptic Density by PSD-95 Serine 73 Phosphorylation Inhibits Spine Growth and Synaptic Plasticity , 2009, Neuron.
[19] W. Klein,et al. N‐Methyl‐d‐aspartate receptors are required for synaptic targeting of Alzheimer’s toxic amyloid‐β peptide oligomers , 2010, Journal of neurochemistry.
[20] S. Love,et al. Premorbid effects of APOE on synaptic proteins in human temporal neocortex , 2006, Neurobiology of Aging.
[21] Shaomin Li,et al. Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory , 2008, Nature Medicine.
[22] Kristina D. Micheva,et al. Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques , 2009, Proceedings of the National Academy of Sciences.
[23] P. Riederer,et al. Functional Neurochemistry of Alzheimers Disease , 2004 .
[24] S. Love,et al. Measurement of pre- and post-synaptic proteins in cerebral cortex: effects of post-mortem delay , 2004, Journal of Neuroscience Methods.
[25] N. Inestrosa,et al. β-Amyloid Causes Depletion of Synaptic Vesicles Leading to Neurotransmission Failure* , 2009, The Journal of Biological Chemistry.
[26] Ning Zhang,et al. Different expression of NR2B and PSD‐95 in rat hippocampal subregions during postnatal development , 2009, Microscopy research and technique.
[27] H. Bading,et al. Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways , 2002, Nature Neuroscience.
[28] A. Buisson,et al. Synapses, NMDA receptor activity and neuronal Aβ production in Alzheimer’s disease , 2011, Reviews in the neurosciences.
[29] M. Constantine‐Paton,et al. BDNF induces transport of PSD-95 to dendrites through PI3K-AKT signaling after NMDA receptor activation , 2007, Nature Neuroscience.
[30] R. Tanzi. The synaptic Aβ hypothesis of Alzheimer disease , 2005, Nature Neuroscience.
[31] Jürgen Götz,et al. Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease , 2011, Nature Reviews Neuroscience.
[32] M. Martín-Satué,et al. Amyloid β peptide oligomers directly activate NMDA receptors. , 2011, Cell calcium.
[33] E B Mukaetova-Ladinska,et al. Staging of cytoskeletal and beta-amyloid changes in human isocortex reveals biphasic synaptic protein response during progression of Alzheimer's disease. , 2000, The American journal of pathology.
[34] C. Bouras,et al. Ubiquitination and cysteine nitrosylation during aging and Alzheimer's disease , 2009, Brain Research Bulletin.
[35] C. Lippa,et al. Review: Disruption of the Postsynaptic Density in Alzheimer’s Disease and Other Neurodegenerative Dementias , 2010, American journal of Alzheimer's disease and other dementias.
[36] Yen-Chung Chang,et al. Heavy chain of cytoplasmic dynein is a major component of the postsynaptic density fraction , 2006, Journal of neuroscience research.
[37] R. Roberts,et al. Dual use of immunohistochemistry for film densitometry and light microscopy , 2012, Journal of Neuroscience Methods.
[38] Eric Tardif,et al. Differential changes in synaptic proteins in the Alzheimer frontal cortex with marked increase in PSD-95 postsynaptic protein. , 2008, Journal of Alzheimer's disease : JAD.
[39] P. Dodd,et al. Reduction in post-synaptic scaffolding PSD-95 and SAP-102 protein levels in the Alzheimer inferior temporal cortex is correlated with disease pathology. , 2010, Journal of Alzheimer's disease : JAD.
[40] E. Mandelkow,et al. Linking Amyloid-β and Tau: Amyloid-β Induced Synaptic Dysfunction via Local Wreckage of the Neuronal Cytoskeleton , 2011, Neurodegenerative Diseases.
[41] Jürgen Götz,et al. Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models , 2010, Cell.
[42] D. Purpura,et al. NMDA receptor trafficking in synaptic plasticity and neuropsychiatric disorders , 2007, Nature Reviews Neuroscience.
[43] V. Nimmrich,et al. Is Alzheimer's Disease a Result of Presynaptic Failure? - Synaptic Dysfunctions Induced by Oligomeric β-Amyloid , 2009, Reviews in the neurosciences.
[44] André Schrattenholz,et al. NMDA receptors are not alone: dynamic regulation of NMDA receptor structure and function by neuregulins and transient cholesterol-rich membrane domains leads to disease-specific nuances of glutamate-signalling. , 2006, Current topics in medicinal chemistry.
[45] M. Constantine‐Paton,et al. Receptor compartmentalization and trafficking at glutamate synapses: a developmental proposal , 2004, Trends in Neurosciences.
[46] Shigeo Okabe,et al. Differential Control of Postsynaptic Density Scaffolds via Actin-Dependent and -Independent Mechanisms , 2006, The Journal of Neuroscience.
[47] G. Leuba,et al. The role of the ubiquitin proteasome system in Alzheimer's disease , 2011, Experimental biology and medicine.
[48] C. Parsons,et al. Alzheimer's disease, β‐amyloid, glutamate, NMDA receptors and memantine – searching for the connections , 2012, British journal of pharmacology.
[49] J. Kaye,et al. Differential loss of synaptic proteins in Alzheimer's disease: implications for synaptic dysfunction. , 2005, Journal of Alzheimer's disease : JAD.
[50] G. Leuba,et al. Postsynaptic density protein PSD-95 expression in Alzheimer's disease and okadaic acid induced neuritic retraction , 2008, Neurobiology of Disease.
[51] M. Sheng,et al. PDZ domain proteins of synapses , 2004, Nature Reviews Neuroscience.
[52] R. Rissman,et al. Biochemical and molecular studies of NMDA receptor subunits NR1/2A/2B in hippocampal subregions throughout progression of Alzheimer's disease pathology , 2004, Neurobiology of Disease.
[53] Ghiam Yamin. NMDA receptor–dependent signaling pathways that underlie amyloid β‐protein disruption of LTP in the hippocampus , 2009, Journal of neuroscience research.
[54] K. Magnusson,et al. Frontiers in Aging Neuroscience Aging Neuroscience Review Article , 2022 .
[55] P. Dodd,et al. Post-synaptic scaffolding protein interactions with glutamate receptors in synaptic dysfunction and Alzheimer's disease , 2011, Progress in Neurobiology.
[56] Tsutomu Hashikawa,et al. Retrograde modulation of presynaptic release probability through signaling mediated by PSD-95–neuroligin , 2007, Nature Neuroscience.
[57] D. Winder,et al. Plasticity and behavior New genetic techniques to address multiple forms and functions , 2001, Physiology & Behavior.
[58] R. Petralia. Distribution of Extrasynaptic NMDA Receptors on Neurons , 2012, TheScientificWorldJournal.