Abstract
Alzheimer's disease is a devastating neurological disorder. The role of hyperexcitability in the disease's cognitive decline is not completely understood. In this issue of Neuron, Palop et al. report both limbic seizures and presumed homeostatic responses to seizures in an animal model of Alzheimer's.
MeSH terms
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Alzheimer Disease / complications
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Alzheimer Disease / physiopathology*
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Amyloid beta-Peptides / metabolism
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Amyloid beta-Protein Precursor / genetics
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Amyloid beta-Protein Precursor / metabolism
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Animals
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Cognition Disorders / etiology
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Cognition Disorders / physiopathology*
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Dentate Gyrus / physiopathology*
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Disease Models, Animal
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Epilepsy / etiology
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Epilepsy / physiopathology*
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Homeostasis / genetics
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Humans
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Mutation / genetics
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Neural Inhibition / genetics
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Neuropeptide Y / metabolism
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Neuropeptide Y