Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain. - Wikidata - awgldk - TriplyDB

Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain.

Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain.

http://www.wikidata.org/entity/Q33510497

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Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model.Emerging Link between Alzheimer's Disease and Homeostatic Synaptic Plasticity The multifaceted nature of amyloid precursor protein and its proteolytic fragments: friends and foes APP intracellular domain impairs adult neurogenesis in transgenic mice by inducing neuroinflammation Tau Protein Mediates APP Intracellular Domain (AICD)-Induced Alzheimer's-Like Pathological Features in Mice DBA/2J genetic background exacerbates spontaneous lethal seizures but lessens amyloid deposition in a mouse model of Alzheimer's disease.Alzheimer's disease and Down syndrome rodent models exhibit audiogenic seizures.Amyloid-β/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's disease.An overview of APP processing enzymes and products.Seizures and epilepsy in Alzheimer's disease p38 MAP kinase-mediated NMDA receptor-dependent suppression of hippocampal hypersynchronicity in a mouse model of Alzheimer's disease Model Hirano bodies protect against tau-independent and tau-dependent cell death initiated by the amyloid precursor protein intracellular domain.Life extension factor klotho prevents mortality and enhances cognition in hAPP transgenic mice.Neurogenin 2 mediates amyloid-β precursor protein-stimulated neurogenesis.Functional α7β2 nicotinic acetylcholine receptors expressed in hippocampal interneurons exhibit high sensitivity to pathological level of amyloid β peptides.The roles of amyloid precursor protein (APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimer disease.The keystone of Alzheimer pathogenesis might be sought in Aβ physiology "Untangling" Alzheimer's disease and epilepsy.Soluble Aβ oligomers impair hippocampal LTP by disrupting glutamatergic/GABAergic balance.Seizure-Induced Regulations of Amyloid-β, STEP61, and STEP61 Substrates Involved in Hippocampal Synaptic Plasticity.Hippocampal oscillatory activity in Alzheimer's disease: toward the identification of early biomarkers?Antisense reduction of tau in adult mice protects against seizures Overexpression of Hsp27 ameliorates symptoms of Alzheimer's disease in APP/PS1 mice.Shared cognitive and behavioral impairments in epilepsy and Alzheimer's disease and potential underlying mechanisms.Differential contribution of APP metabolites to early cognitive deficits in a TgCRND8 mouse model of Alzheimer's disease.Importance of the caspase cleavage site in amyloid-β protein precursor Amyloid-independent mechanisms in Alzheimer's disease pathogenesis The physiology of the β-amyloid precursor protein intracellular domain AICD.Neurodegeneration in Alzheimer disease: role of amyloid precursor protein and presenilin 1 intracellular signaling.Neurotoxicity of amyloid β-protein: synaptic and network dysfunction.Wnts in adult brain: from synaptic plasticity to cognitive deficiencies.The dark sides of amyloid in Alzheimer's disease pathogenesis.Antiepileptics topiramate and levetiracetam alleviate behavioral deficits and reduce neuropathology in APPswe/PS1dE9 transgenic mice.Epileptic activity in Alzheimer's disease: causes and clinical relevance.Targeting Neural Hyperactivity as a Treatment to Stem Progression of Late-Onset Alzheimer's Disease.The SHH/Gli pathway is reactivated in reactive glia and drives proliferation in response to neurodegeneration-induced lesions.The amyloid precursor protein intracellular domain-fe65 multiprotein complexes: a challenge to the amyloid hypothesis for Alzheimer's disease?Aging and excitotoxic stress exacerbate neural circuit reorganization in amyloid precursor protein intracellular domain transgenic mice Corticothalamic network dysfunction and behavioral deficits in a mouse model of Alzheimer's disease.Different Scales of Cortical Organization are Selectively Targeted in the Progression to Alzheimer's Disease.

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Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain.

http://www.wikidata.org/entity/Q33510497

description

2009 nî lūn-bûn

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2009 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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Abnormal neuronal networks and ...... the APP intracellular domain.

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Abnormal neuronal networks and ...... the APP intracellular domain.

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Abnormal neuronal networks and ...... the APP intracellular domain.

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Abnormal neuronal networks and ...... the APP intracellular domain.

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Abnormal neuronal networks and ...... the APP intracellular domain.

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Abnormal neuronal networks and ...... the APP intracellular domain.

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J.NEUROBIOLAGING.2009.09.002

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Neurobiology of Aging

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Abnormal neuronal networks and ...... g the APP intracellular domain

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B T Lamb

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D E Bredesen

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D Thomas

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S W Pimplikar

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P2860

Familial Alzheimer's disease mutations inhibit gamma-secretase-mediated liberation of beta-amyloid precursor protein carboxy-terminal fragment

Fe65 and the protein network centered around the cytosolic domain of the Alzheimer's beta-amyloid precursor protein

Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease

beta Subunits of voltage-gated sodium channels are novel substrates of beta-site amyloid precursor protein-cleaving enzyme (BACE1) and gamma-secretase.

Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664.

Down syndrome, Alzheimer's disease and seizures.

Activation of GSK-3 and phosphorylation of CRMP2 in transgenic mice expressing APP intracellular domain.

Evidence that the Amyloid beta Precursor Protein-intracellular domain lowers the stress threshold of neurons and has a "regulated" transcriptional role

The FE65 proteins and Alzheimer's disease.

The GSK3 hypothesis of Alzheimer's disease

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