about
C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal traffickingConnectivity of Pathology: The Olfactory System as a Model for Network-Driven Mechanisms of Alzheimer's Disease PathogenesisEnvironmental novelty exacerbates stress hormones and Aβ pathology in an Alzheimer's model.Microfluidic culture platform for studying neuronal response to mild to very mild axonal stretch injury.Diffuse axonal injury in brain trauma: insights from alterations in neurofilaments.Stainless steel pinholes for fast fabrication of high-performance microchip electrophoresis devices by CO2 laser ablation.Identifying the primary site of pathogenesis in amyotrophic lateral sclerosis - vulnerability of lower motor neurons to proximal excitotoxicity.C9ORF72 expression and cellular localization over mouse development.Mild and repetitive very mild axonal stretch injury triggers cystoskeletal mislocalization and growth cone collapse.ALS-associated mutant FUS inhibits macroautophagy which is restored by overexpression of Rab1Excitotoxin-induced caspase-3 activation and microtubule disintegration in axons is inhibited by taxol.Axonopathy and cytoskeletal disruption in degenerative diseases of the central nervous system.Calretinin and Neuropeptide Y interneurons are differentially altered in the motor cortex of the SOD1G93A mouse model of ALS.Microglia and motor neurons during disease progression in the SOD1G93A mouse model of amyotrophic lateral sclerosis: changes in arginase1 and inducible nitric oxide synthase.Excitotoxicity in ALS: Overstimulation, or overreaction?Rab1-dependent ER-Golgi transport dysfunction is a common pathogenic mechanism in SOD1, TDP-43 and FUS-associated ALS.Excitotoxicity mediated by non-NMDA receptors causes distal axonopathy in long-term cultured spinal motor neurons.Alzheimer's Disease and NQO1: Is there a Link?Microfluidic primary culture model of the lower motor neuron-neuromuscular junction circuit.Cortical murine neurons lacking the neurofilament light chain protein have an attenuated response to injury in vitro.Axonal degeneration, distal collateral branching and neuromuscular junction architecture alterations occur prior to symptom onset in the SOD1(G93A) mouse model of amyotrophic lateral sclerosis.AAV-Mediated CRISPR/Cas Gene Editing of Retinal Cells In Vivo.Combination treatment with leptin and pioglitazone in a mouse model of Alzheimer's disease.Cytoskeletal alterations differentiate presenilin-1 and sporadic Alzheimer's disease.Retinal ganglion cell axons regenerate in the presence of intact sensory fibres.α-Synuclein protects neurons from apoptosis downstream of free-radical production through modulation of the MAPK signalling pathway.Methods for In Vivo CRISPR/Cas Editing of the Adult Murine Retina.AAV-mediated gene delivery of the calreticulin anti-angiogenic domain inhibits ocular neovascularization.Neuroprotective upregulation of endogenous α-synuclein precedes ubiquitination in cultured dopaminergic neurons.The effect of focal brain injury on beta-amyloid plaque deposition, inflammation and synapses in the APP/PS1 mouse model of Alzheimer's disease.Mid-life environmental enrichment increases synaptic density in CA1 in a mouse model of Aβ-associated pathology and positively influences synaptic and cognitive health in healthy ageing.Changes in TDP-43 expression in development, aging, and in the neurofilament light protein knockout mouse.Alterations in neurofilaments and the transformation of the cytoskeleton in axons may provide insight into the aberrant neuronal changes of Alzheimer's disease.Localization of glutamate receptors in developing cortical neurons in culture and relationship to susceptibility to excitotoxicity.Peripheral treatment with enoxaparin exacerbates amyloid plaque pathology in Tg2576 mice.The impact of metallothionein-II on microglial response to tumor necrosis factor-alpha (TNFα) and downstream effects on neuronal regeneration.Alpha-synuclein is upregulated in neurones in response to chronic oxidative stress and is associated with neuroprotection.Neurofilament light gene deletion exacerbates amyloid, dystrophic neurite, and synaptic pathology in the APP/PS1 transgenic model of Alzheimer's disease.Amyloid β accumulation and inner retinal degenerative changes in Alzheimer's disease transgenic mouse.The HDAC6 Inhibitor Trichostatin A Acetylates Microtubules and Protects Axons From Excitotoxin-Induced Degeneration in a Compartmented Culture Model
P50
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P50
description
hulumtuese
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researcher
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wetenschapper
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հետազոտող
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name
Anna E. King
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Anna E. King
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Anna E. King
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Anna E. King
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Anna E. King
@sl
آنا إي. كينغ
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type
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Anna E. King
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Anna E. King
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Anna E. King
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Anna E. King
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Anna E. King
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آنا إي. كينغ
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A.E.King
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Anna E. King
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Anna Elizabeth King
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Anna E. King
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Anna E. King
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Anna E. King
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Anna E. King
@nl
Anna E. King
@sl
آنا إي. كينغ
@ar
P1053
J-7927-2014
P106
P1153
55451508900
P21
P31
P3829
P496
0000-0003-1792-0965