Alzheimer brain-derived amyloid β-protein impairs synaptic remodeling and memory consolidation

[1]  D. Holtzman,et al.  The levels of water-soluble and triton-soluble Aβ are increased in Alzheimer's disease brain , 2012, Brain Research.

[2]  D. Selkoe,et al.  Aβ oligomers inhibit synapse remodelling necessary for memory consolidation , 2011, Neurobiology of Aging.

[3]  K. J. Murphy,et al.  Temporal proteomic profile of memory consolidation in the rat hippocampal dentate gyrus , 2011, Proteomics.

[4]  K. Ashe,et al.  Cognitive effects of cell-derived and synthetically derived Aβ oligomers , 2011, Neurobiology of Aging.

[5]  M. Rowan,et al.  Interaction between prion protein and toxic amyloid β assemblies can be therapeutically targeted at multiple sites , 2011, Nature communications.

[6]  M. Rowan,et al.  Alzheimer's Disease Brain-Derived Amyloid-β-Mediated Inhibition of LTP In Vivo Is Prevented by Immunotargeting Cellular Prion Protein , 2011, The Journal of Neuroscience.

[7]  J. Valero,et al.  The role of CREB signaling in Alzheimer’s disease and other cognitive disorders , 2011, Reviews in the neurosciences.

[8]  N. Ferguson,et al.  Amyloid β-Protein Dimers Rapidly Form Stable Synaptotoxic Protofibrils , 2010, The Journal of Neuroscience.

[9]  D. Walsh,et al.  Macroautophagy Is Not Directly Involved in the Metabolism of Amyloid Precursor Protein* , 2010, The Journal of Biological Chemistry.

[10]  Asad Jan,et al.  Preparation and characterization of toxic Aβ aggregates for structural and functional studies in Alzheimer's disease research , 2010, Nature Protocols.

[11]  D. Selkoe,et al.  The presence of sodium dodecyl sulphate-stable Abeta dimers is strongly associated with Alzheimer-type dementia. , 2010, Brain : a journal of neurology.

[12]  B. Strooper.  Proteases and Proteolysis in Alzheimer Disease: A Multifactorial View on the Disease Process , 2010 .

[13]  S. Strittmatter,et al.  β-amyloid oligomers and cellular prion protein in Alzheimer’s disease , 2010, Journal of Molecular Medicine.

[14]  D. Selkoe,et al.  β‐Secretase cleavage is not required for generation of the intracellular C‐terminal domain of the amyloid precursor family of proteins , 2010, The FEBS journal.

[15]  D. Selkoe,et al.  Biochemical and immunohistochemical analysis of an Alzheimer's disease mouse model reveals the presence of multiple cerebral Aβ assembly forms throughout life , 2009, Neurobiology of Disease.

[16]  V. Perry,et al.  Selective presynaptic degeneration in the synaptopathy associated with ME7-induced hippocampal pathology , 2009, Neurobiology of Disease.

[17]  Shaomin Li,et al.  Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate Uptake , 2009, Neuron.

[18]  Cindee M. Madison,et al.  Episodic memory loss is related to hippocampal-mediated beta-amyloid deposition in elderly subjects. , 2009, Brain : a journal of neurology.

[19]  John W. Gilbert,et al.  Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-β Oligomers , 2009, Nature.

[20]  M. Segal,et al.  Synaptopodin Regulates Plasticity of Dendritic Spines in Hippocampal Neurons , 2009, The Journal of Neuroscience.

[21]  M. Prince.  The 10/66 dementia research group - 10 years on , 2009, Indian journal of psychiatry.

[22]  K. J. Murphy,et al.  Intraventricular infusions of anti–NCAM PSA impair the process of consolidation of both avoidance conditioning and spatial learning paradigms in Wistar rats , 2008, Neuroscience.

[23]  A. Poling,et al.  Oligomers of the amyloid-β protein disrupt working memory: Confirmation with two behavioral procedures , 2008, Behavioural Brain Research.

[24]  Andreas Vlachos,et al.  A role for the spine apparatus in LTP and spatial learning , 2008, Behavioural Brain Research.

[25]  S. Scheff,et al.  Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury. , 2008, Free radical biology & medicine.

[26]  Shaomin Li,et al.  Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory , 2008, Nature Medicine.

[27]  T. Casoli,et al.  Synaptic remodeling in hippocampal CA1 region of aged rats correlates with better memory performance in passive avoidance test. , 2008, Rejuvenation research.

[28]  W. K. Cullen,et al.  Amyloid β Protein Dimer-Containing Human CSF Disrupts Synaptic Plasticity: Prevention by Systemic Passive Immunization , 2008, The Journal of Neuroscience.

[29]  R. Lipton,et al.  Memory impairment, executive dysfunction, and intellectual decline in preclinical Alzheimer's disease , 2008, Journal of the International Neuropsychological Society.

[30]  N. Hooper,et al.  Cellular prion protein regulates β-secretase cleavage of the Alzheimer's amyloid precursor protein , 2007, Proceedings of the National Academy of Sciences.

[31]  K. J. Murphy,et al.  Temporal change in gene expression in the rat dentate gyrus following passive avoidance learning , 2007, Journal of neurochemistry.

[32]  F. Schmitt,et al.  Synaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment , 2007, Neurology.

[33]  R. Berry,et al.  β-Site Amyloid Precursor Protein Cleaving Enzyme 1 Levels Become Elevated in Neurons around Amyloid Plaques: Implications for Alzheimer's Disease Pathogenesis , 2007, The Journal of Neuroscience.

[34]  D. Selkoe,et al.  The APP family of proteins: similarities and differences. , 2007, Biochemical Society transactions.

[35]  R. Malinow,et al.  PSD-95 is required for activity-driven synapse stabilization , 2007, Proceedings of the National Academy of Sciences.

[36]  Diano F. Marrone,et al.  Ultrastructural plasticity associated with hippocampal-dependent learning: A meta-analysis , 2007, Neurobiology of Learning and Memory.

[37]  M. Frotscher,et al.  A role for synaptopodin and the spine apparatus in hippocampal synaptic plasticity. , 2007, Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft.

[38]  M. Bennett,et al.  PSD-95 and PKC converge in regulating NMDA receptor trafficking and gating , 2006, Proceedings of the National Academy of Sciences.

[39]  F. Schmitt,et al.  Hippocampal synaptic loss in early Alzheimer's disease and mild cognitive impairment , 2006, Neurobiology of Aging.

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

[41]  C. Mathers,et al.  Global prevalence of dementia: a Delphi consensus study , 2005, The Lancet.

[42]  K. J. Murphy,et al.  Amyloid precursor protein expression in the rat hippocampal dentate gyrus modulates during memory consolidation , 2005, Journal of neurochemistry.

[43]  E. Masliah,et al.  β-Amyloid Immunotherapy Prevents Synaptic Degeneration in a Mouse Model of Alzheimer's Disease , 2005, The Journal of Neuroscience.

[44]  Morris Moscovitch,et al.  Where to? Remote Memory for Spatial Relations and Landmark Identity in Former Taxi Drivers with Alzheimer's Disease and Encephalitis , 2005, Journal of Cognitive Neuroscience.

[45]  E. Kandel.  The Molecular Biology of Memory Storage: A Dialog Between Genes and Synapses , 2004, Bioscience Reports.

[46]  Jesus Avila,et al.  Role of tau protein in both physiological and pathological conditions. , 2004, Physiological reviews.

[47]  P. Coleman,et al.  Synaptic slaughter in Alzheimer’s disease , 2003, Neurobiology of Aging.

[48]  S. Scheff,et al.  Synaptic pathology in Alzheimer’s disease: a review of ultrastructural studies , 2003, Neurobiology of Aging.

[49]  D. Holtzman,et al.  In Vivo Assessment of Brain Interstitial Fluid with Microdialysis Reveals Plaque-Associated Changes in Amyloid-β Metabolism and Half-Life , 2003, The Journal of Neuroscience.

[50]  K. Willecke,et al.  Connexin30‐deficient mice show increased emotionality and decreased rearing activity in the open‐field along with neurochemical changes , 2003, The European journal of neuroscience.

[51]  Avi Avital,et al.  Morphological changes in hippocampal dentate gyrus synapses following spatial learning in rats are transient , 2003, The European journal of neuroscience.

[52]  P. Coleman,et al.  Defects in expression of genes related to synaptic vesicle traffickingin frontal cortex of Alzheimer’s disease , 2003, Neurobiology of Disease.

[53]  D. Selkoe.  Alzheimer's Disease Is a Synaptic Failure , 2002, Science.

[54]  W. K. Cullen,et al.  Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.

[55]  M. Sheng,et al.  Dentritic spines : structure, dynamics and regulation , 2001, Nature Reviews Neuroscience.

[56]  E. Kandel.  The Molecular Biology of Memory Storage: A Dialogue Between Genes and Synapses , 2001, Science.

[57]  H. Annoura,et al.  Progressive brain dysfunction following intracerebroventricular infusion of beta1–42-amyloid peptide , 2001, Brain Research.

[58]  H. Gundersen,et al.  Total regional and global number of synapses in the human brain neocortex , 2001, Synapse.

[59]  C. Finch,et al.  Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum? , 2001, Trends in Neurosciences.

[60]  E. Masliah,et al.  Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease , 2001, Neurology.

[61]  Gary W. Small,et al.  Early diagnosis of Alzheimer's disease: update on combining genetic and brain-imaging measures , 2000, Dialogues in clinical neuroscience.

[62]  V. Berezin,et al.  A Synthetic Peptide Ligand of Neural Cell Adhesion Molecule (NCAM) IgI Domain Prevents NCAM Internalization and Disrupts Passive Avoidance Learning , 2000, Journal of neurochemistry.

[63]  J. Ávila,et al.  Phosphorylation of microtubule-associated protein 2 (MAP2) and its relevance for the regulation of the neuronal cytoskeleton function , 2000, Progress in Neurobiology.

[64]  C. Masters,et al.  Soluble pool of Aβ amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease , 1999, Annals of neurology.

[65]  M. Mesulam.  Neuroplasticity Failure in Alzheimer's Disease Bridging the Gap between Plaques and Tangles , 1999, Neuron.

[66]  L. Lue,et al.  Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease , 1999 .

[67]  R. Mayeux,et al.  Differential regional dysfunction of the hippocampal formation among elderly with memory decline and Alzheimer's disease , 1999, Annals of neurology.

[68]  L. Squire,et al.  100 years of consolidation--remembering Müller and Pilzecker. , 1999, Learning & memory.

[69]  C. Regan,et al.  Ultrastructural analysis reveals avoidance conditioning to induce a transient increase in hippocampal dentate spine density in the 6hour post-training period of consolidation , 1998, Neuroscience.

[70]  K. J. Murphy,et al.  Contributions of Cell Adhesion Molecules to Altered Synaptic Weightings during Memory Consolidation , 1998, Neurobiology of Learning and Memory.

[71]  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.

[72]  S. Sara,et al.  Neural cell adhesion molecules play a role in rat memory formation in appetitive as well as aversive tasks , 1997, Neuroreport.

[73]  S. Rose,et al.  Antibody to Day-Old Chick Brain Glycoprotein Produces Amnesia in Adult Rats , 1997, Neurobiology of Learning and Memory.

[74]  M. Ball,et al.  Water-soluble A(N-40, N-42) Oligomers in Normal and Alzheimer Disease Brains (*) , 1996, The Journal of Biological Chemistry.

[75]  M. Tabaton,et al.  Soluble amyloid beta-protein is a marker of Alzheimer amyloid in brain but not in cerebrospinal fluid. , 1994, Biochemical and biophysical research communications.

[76]  C. Regan,et al.  Intraventricular Infusions of Anti‐Neural Cell Adhesion Molecules in a Discrete Posttraining Period Impair Consolidation of a Passive Avoidance Response in the Rat , 1992, Journal of neurochemistry.

[77]  E. Masliah,et al.  Immunohistochemical quantification of the synapse-related protein synaptophysin in Alzheimer disease , 1989, Neuroscience Letters.

[78]  P. Landfield,et al.  Synaptic vesicle redistribution during hippocampal frequency potentiation and depression in young and aged rats , 1988, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[79]  K. Kosik,et al.  Axonal disruption and aberrant localization of tau protein characterize the neuropil pathology of Alzheimer's disease , 1987, Annals of neurology.

[80]  D. Mann,et al.  A quantitative morphometric analysis of the neuronal and synaptic content of the frontal and temporal cortex in patients with Alzheimer's disease , 1987, Journal of the Neurological Sciences.

[81]  P. Knaus,et al.  Expression of Synaptophysin During Postnatal Development of the Mouse Brain , 1986, Journal of neurochemistry.

[82]  L. Squire,et al.  Protein synthesis and memory: a review. , 1984, Psychological bulletin.

[83]  D. C. Sterio.  The unbiased estimation of number and sizes of arbitrary particles using the disector , 1984, Journal of microscopy.

[84]  I. Evangelista,et al.  THE CONTRIBUTION OF ALTERED SYNAPSES IN THE SENILE PLAQUE: AN ELECTRON MICROSCOPIC STUDY IN ALZHEIMER'S DEMENTIA , 1967, Journal of neuropathology and experimental neurology.

[85]  E. Klann,et al.  Making synaptic plasticity and memory last: mechanisms of translational regulation. , 2009, Genes & development.

[86]  Manuel Buttini,et al.  Mice as models: transgenic approaches and Alzheimer's disease. , 2006, Journal of Alzheimer's disease : JAD.

[87]  D. Selkoe,et al.  Natural oligomers of the amyloid-β protein specifically disrupt cognitive function , 2005, Nature Neuroscience.

[88]  J. Kaye,et al.  Differential loss of synaptic proteins in Alzheimer's disease: implications for synaptic dysfunction. , 2005, Journal of Alzheimer's disease : JAD.

[89]  Joseph E LeDoux,et al.  Structural plasticity and memory , 2004, Nature Reviews Neuroscience.

[90]  Alcino J. Silva,et al.  CREB and memory. , 1998, Annual review of neuroscience.

[91]  G. Paxinos,et al.  The Rat Brain in Stereotaxic Coordinates , 1983 .

[92]  D. Walsh,et al.  Molecular Neurodegeneration Alzheimer's Disease: Synaptic Dysfunction and Aβ , 2022 .