Aβ oligomers from human brain impair mossy fiber LTP in CA3 of hippocampus, but activating cAMP-PKA and cGMP-PKG prevents this
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[1] Yoav Ben-Simon,et al. cAMP-Dependent Synaptic Plasticity at the Hippocampal Mossy Fiber Terminal , 2022, Frontiers in Synaptic Neuroscience.
[2] D. Selkoe,et al. An ultra‐sensitive immunoassay detects and quantifies soluble Aβ oligomers in human plasma , 2021, Alzheimer's & dementia : the journal of the Alzheimer's Association.
[3] M. Kennedy,et al. Verubecestat for Prodromal Alzheimer's Disease. Reply. , 2019, The New England journal of medicine.
[4] Elentina K. Argyrousi,et al. Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade , 2019, Molecular Neurodegeneration.
[5] Shaomin Li,et al. Decoding the synaptic dysfunction of bioactive human AD brain soluble Aβ to inspire novel therapeutic avenues for Alzheimer’s disease , 2018, Acta Neuropathologica Communications.
[6] A. Palmeri,et al. The effect of amyloid-β peptide on synaptic plasticity and memory is influenced by different isoforms, concentrations, and aggregation status , 2018, Neurobiology of Aging.
[7] M. Frosch,et al. Diffusible, highly bioactive oligomers represent a critical minority of soluble Aβ in Alzheimer’s disease brain , 2018, Acta Neuropathologica.
[8] W. Klein,et al. A human scFv antibody that targets and neutralizes high molecular weight pathogenic amyloid‐β oligomers , 2017, Journal of neurochemistry.
[9] C. Mulle,et al. PGE2-EP3 signaling pathway impairs hippocampal presynaptic long-term plasticity in a mouse model of Alzheimer's disease , 2017, Neurobiology of Aging.
[10] Shaomin Li,et al. Large Soluble Oligomers of Amyloid β-Protein from Alzheimer Brain Are Far Less Neuroactive Than the Smaller Oligomers to Which They Dissociate , 2017, The Journal of Neuroscience.
[11] M. Rowan,et al. Peripheral Interventions Enhancing Brain Glutamate Homeostasis Relieve Amyloid &bgr;- and TNF&agr;- Mediated Synaptic Plasticity Disruption in the Rat Hippocampus , 2016, Cerebral cortex.
[12] Denise Manahan-Vaughan,et al. β-Adrenergic Control of Hippocampal Function: Subserving the Choreography of Synaptic Information Storage and Memory , 2016, Cerebral cortex.
[13] O. Arancio,et al. Synaptic Therapy in Alzheimer’s Disease: A CREB-centric Approach , 2015, Neurotherapeutics.
[14] E. Rolls. A quantitative theory of the functions of the hippocampal CA3 network in memory , 2013, Front. Cell. Neurosci..
[15] J. Corbin,et al. Mammalian cyclic nucleotide phosphodiesterases: molecular mechanisms and physiological functions. , 2011, Physiological reviews.
[16] Richard Graham Knowles,et al. GSK256066, an Exceptionally High-Affinity and Selective Inhibitor of Phosphodiesterase 4 Suitable for Administration by Inhalation: In Vitro, Kinetic, and In Vivo Characterization , 2011, Journal of Pharmacology and Experimental Therapeutics.
[17] D. Selkoe,et al. Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration , 2011, Proceedings of the National Academy of Sciences.
[18] Matthew W. Jones,et al. Altered synaptic plasticity in the mossy fibre pathway of transgenic mice expressing mutant amyloid precursor protein , 2010, Molecular Brain.
[19] Shaomin Li,et al. Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory , 2008, Nature Medicine.
[20] N. Lemon,et al. Beta-adrenergic receptor activation during distinct patterns of stimulation critically modulates the PKA-dependence of LTP in the mouse hippocampus. , 2008, Learning & memory (Cold Spring Harbor, N.Y.).
[21] Susumu Tonegawa,et al. Transgenic Inhibition of Synaptic Transmission Reveals Role of CA3 Output in Hippocampal Learning , 2008, Science.
[22] R. Kesner. Behavioral functions of the CA3 subregion of the hippocampus. , 2007, Learning & memory.
[23] J. Beavo,et al. Cyclic Nucleotide Phosphodiesterases: Molecular Regulation to Clinical Use , 2006, Pharmacological Reviews.
[24] O. Vitolo,et al. Ubiquitin Hydrolase Uch-L1 Rescues β-Amyloid-Induced Decreases in Synaptic Function and Contextual Memory , 2006, Cell.
[25] Dietmar Schmitz,et al. Synaptic plasticity at hippocampal mossy fibre synapses , 2005, Nature Reviews Neuroscience.
[26] A. Palmeri,et al. Amyloid-β Peptide Inhibits Activation of the Nitric Oxide/cGMP/cAMP-Responsive Element-Binding Protein Pathway during Hippocampal Synaptic Plasticity , 2005, The Journal of Neuroscience.
[27] R. Kesner,et al. Differential contributions of dorsal hippocampal subregions to memory acquisition and retrieval in contextual fear‐conditioning , 2004, Hippocampus.
[28] M. Quirk,et al. Hippocampal CA3 NMDA Receptors Are Crucial for Memory Acquisition of One-Time Experience , 2003, Neuron.
[29] D. Selkoe. Alzheimer's Disease Is a Synaptic Failure , 2002, Science.
[30] O. Vitolo,et al. Amyloid β-peptide inhibition of the PKA/CREB pathway and long-term potentiation: Reversibility by drugs that enhance cAMP signaling , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[31] M. Min,et al. Change in bi‐directional plasticity at CA1 synapses in hippocampal slices taken from 6‐hydroxydopamine‐treated rats: the role of endogenous norepinephrine , 2002, The European journal of neuroscience.
[32] G. Buzsáki,et al. Single granule cells reliably discharge targets in the hippocampal CA3 network in vivo , 2002, Nature Neuroscience.
[33] W. K. Cullen,et al. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.
[34] Brett Chromy,et al. Soluble oligomers of β amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus , 2002, Brain Research.
[35] C. Masters,et al. Soluble pool of Aβ amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease , 1999, Annals of neurology.
[36] L. Lue,et al. Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease , 1999 .
[37] E. Kandel,et al. Rolipram, a type IV-specific phosphodiesterase inhibitor, facilitates the establishment of long-lasting long-term potentiation and improves memory. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[38] 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.
[39] Paul Antoine Salin,et al. Distinct short-term plasticity at two excitatory synapses in the hippocampus. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[40] E. Kandel,et al. Modulation of Both the Early and the Late Phase of Mossy Fiber LTP by the Activation of β-Adrenergic Receptors , 1996, Neuron.
[41] D. Johnston,et al. Noradrenergic enhancement of long-term potentiation at mossy fiber synapses in the hippocampus. , 1988, Journal of neurophysiology.