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Bin Cheng
Researcher at University of Kentucky
Publications - 19
Citations - 6885
Bin Cheng is an academic researcher from University of Kentucky. The author has contributed to research in topics: Glutamate receptor & Neurotrophic factors. The author has an hindex of 19, co-authored 19 publications receiving 6800 citations.
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beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity
TL;DR: The hypothesis that beta-amyloid can destabilize neuronal calcium regulation and render neurons more vulnerable to environmental stimuli that elevate intracellular calcium levels is tested.
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Estrogens Attenuate and Corticosterone Exacerbates Excitotoxicity, Oxidative Injury, and Amyloid β‐Peptide Toxicity in Hippocampal Neurons
TL;DR: It is concluded that estrogens, progesterone, and corticosterone can directly affect neuronal vulnerability to excitotoxic, metabolic, and oxidative insults, suggesting roles for these steroids in several different neurodegenerative disorders.
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Evidence for excitoprotective and intraneuronal calcium-regulating roles for secreted forms of the β-amyloid precursor protein
TL;DR: It is reported that APPss have a potent neuroprotective action in cultured rat hippocampal and septal neurons and in human cortical neurons, and the neuroprotection was abolished by antibodies to a specific region common to both APPs695 and APPs751.
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Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis
TL;DR: It is reported that TNF beta and TNF alpha can protect cultured embryonic rat hippocampal, septal, and cortical neurons against glucose deprivation-induced injury and excitatory amino acid toxicity, suggesting a neuroprotective role for TNFs in the brain's response to injury.
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β-Amyloid precursor protein metabolites and loss of neuronal Ca2+ homeostasis in Alzheimer's disease
Mark P. Mattson,Steven W. Barger,Bin Cheng,Ivan Lieberburg,Virginia L. Smith-Swintosky,Russell E. Rydel +5 more
TL;DR: Secreted forms of β-amyloid precursor protein are released in response to electrical activity and can modulate neuronal responses to glutamate, suggesting roles in developmental and synaptic plasticity.