APP processing and synaptic function.

By F. Kamenetz, T. Tomita, Helen Hsieh, G. Seabrook, D. Borchelt, T. Iwatsubo, Sangram S. Sisodia, R. Malinow. Neuron, 2003

1,647 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/4e3f191670f451820caf73aef9c8ea20ddec1583

Citations in the corpus

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide (2007, neutral): “Naturally secreted monomeric and oligomeric Aβ species are being characterized in experiments in vivo to decipher their effects on synaptic structure and functio”
Picomolar amyloid-β positively modulates synaptic plasticity and memory in hippocampus (2008, neutral): “Results Picomolar concentrations of A 42 enhance hippocampal long-term potentiation Given that extracellular A levels are likely to be regulated by synaptic activity (Kamenetz et al., 2003; Cirrito et al., 2005), we speculated that A is normally involved in hippocampal LTP, the dominant model of act”
Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, neutral): “Aβ is produced predominantly in endosomes and its release from neurons is modulated by synaptic activity (Kamenetz et al., 2003; Wei et al., 2010) both presynaptically (Cirrito et al.”
The role of microglia in amyloid clearance from the AD brain (2010, neutral): “Ab is secreted from neurons as a consequence of normal synaptic transmis- sion (Cirrito et al. 2005; Kamenetz et al. 2003).”
Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease (2009, neutral): “A is a homeostatic regulator of synaptic strength (Kamenetz et al., 2003), suggesting that perturbations in soluble A levels might be linked to the learning and memory deficits in AD patients (Masliah et al., 2001).”
Linking Lipids to Alzheimer’s Disease: Cholesterol and Beyond (2011, neutral): “Synapses are particularly affected, not only because they are major sites of amyloid-β release but also because amyloid-β release itself is enhanced by synaptic activit”
Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, neutral): “In addition to a physiological role for APP, the Aβ peptide itself plays an important role in synaptic physiology, regulating synaptic scaling (Kamenetz et al. 2003) and synaptic vesicle release (Abramov et al. 2009).”
Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase (2004, neutral): “In hippocampal slice cultures, Kamenetz et al. ( 71 ) recently demonstrated that neuronal activity can influence the secretion of Ab into the extracellular space.”
Alzheimer’s Disease: The Challenge of the Second Century (2011, neutral): “A clue to the relative specificity for Ab deposition in this network may be the fact that this network has the highest baseline neuronal activity in the resting state and that Ab levels are regulated by neuronal activity (40, 41).”
The cell biology of synaptic plasticity: AMPA receptor trafficking. (2007, neutral): “Aβ secretion in vivo is modulated by neuronal activity and depresses both AMPA and NMDA currents in slices (Cirrito et al. 2005, Kamenetz et al. 2003, Snyder et al. 2005).”
Regulation of NMDA receptor trafficking by amyloid-β (2005, neutral): “Results Amyloid-β decreases surface expression of NMDA receptors Low amounts of secreted soluble amyloid-β regulate glutamatergic currents mediated by both NMDA and AMPA receptors without affecting GABA receptor current”
Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. (2007, neutral): “…data are consistent with the growing literature suggesting that A b induces impairments in synaptic glutamatergic transmission and retraction of excitatory dendritic spines (Hsia et al., 1999; Hsieh et al., 2006; Kamenetz et al., 2003; Palop et al., 2005; Shankar et al., 2007; Walsh et al., 2002).”