Clusters of Hyperactive Neurons Near Amyloid Plaques in a Mouse Model of Alzheimer's Disease
By M. Busche, G. Eichhoff, H. Adelsberger, D. Abramowski, K. Wiederhold, Christian Haass, M. Staufenbiel, Arthur Konnerth, O. Garaschuk. Science, 2008
1,069 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/97dccdb90baa2d61b0ceeb0615ba827154e49532
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In Cellular and Molecular Neuroscience
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Citations in the corpus
- Amyloid β-Induced Neuronal Hyperexcitability Triggers Progressive Epilepsy (2009, background): “These alterations were similar to those induced by excitotoxic stimuli and likely counteracted an initial neuronal overexcitability in corticolimbic neuronal networks (Palop et al., 2007; Busche et al., 2008).”
- Amyloid deposition is associated with impaired default network function in older persons without dementia (2009, neutral): “A recent mouse study suggests that the presence of amyloid plaques may result in abnormally increased neuronal activity in surrounding neurons (Busche et al., 2008).”
- Brain imaging in Alzheimer disease. (2012, background): “…cholinergic or other neurotransmitter up-regulation (DeKosky et al. 2002), aberrant sprouting of cholinergic fibers (Masliah et al. 2003), inefficiency in synaptic transmission (Stern et al. 2004), increased calcium influx, and evidence of excitotoxicity (Palop et al. 2007; Busche et al. 2008).”
- Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models. (2010, positive): “A b -induced aberrant excitatory neuronal activity may contribute to the deficits that characterize AD mouse models (Busche et al., 2008; Palop and Mucke, 2009).”
- Neurotoxicity of amyloid β-protein: synaptic and network dysfunction. (2012, background): “Direct evidence for such fluctuations comes from studies monitoring neuronal expression of the activity-related gene product Arc in dentate granule cells or calcium fluxes in neocortical neurons of live hAPP mice (Palop et al. 2007; Busche et al. 2008).”
- Critical role of soluble amyloid-β for early hippocampal hyperactivity in a mouse model of Alzheimer’s disease (2012, methodology): “For example, in transgenic mice overexpressing both mutant human amyloid precursor protein (APP) and mutant human presenilin 1 (PS1), half of the neurons in layer 2/3 of the cortex were functionally impaired, with a decrease in neuronal activity in 29% of the neurons (termed “silent” neurons) and a ”
- Physiological release of endogenous tau is stimulated by neuronal activity (2013, neutral): “Interestingly, clusters of hyperactive neurons are detected in proximity to plaques in the brain of a mouse model of Alzheimer’s disease in which mutant forms of APP and presenilin-1 are expressed [27].”