Transgenic SOD1 G93A mice develop reduced GLT-1 in spinal cord without alterations in cerebrospinal fluid glutamate levels.
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Chronic Glutamate Toxicity in Neurodegenerative Diseases-What is the Evidence?ALS Patient Stem Cells for Unveiling Disease Signatures of Motoneuron Susceptibility: Perspectives on the Deadly Mitochondria, ER Stress and Calcium TriadElusive roles for reactive astrocytes in neurodegenerative diseasesCurrent approaches to enhance glutamate transporter function and expressionProtein nitration in a mouse model of familial amyotrophic lateral sclerosis: possible multifunctional role in the pathogenesis.Nordihydroguaiaretic acid increases glutamate uptake in vitro and in vivo: therapeutic implications for amyotrophic lateral sclerosisGene profiling of human induced pluripotent stem cell-derived astrocyte progenitors following spinal cord engraftment.Human glial progenitor engraftment and gene expression is independent of the ALS environmentAltered Metabolic Profiles Associate with Toxicity in SOD1G93A Astrocyte-Neuron Co-Cultures.Glutamate transporters and the excitotoxic path to motor neuron degeneration in amyotrophic lateral sclerosis.Optimised and rapid pre-clinical screening in the SOD1(G93A) transgenic mouse model of amyotrophic lateral sclerosis (ALS).Mitochondrial dysfunction and intracellular calcium dysregulation in ALSRiluzole neuroprotection in a Parkinson's disease model involves suppression of reactive astrocytosis but not GLT-1 regulationGlutamate transporter EAAT2: a new target for the treatment of neurodegenerative diseases.Changes in the astrocytic aquaporin-4 and inwardly rectifying potassium channel expression in the brain of the amyotrophic lateral sclerosis SOD1(G93A) rat model.Early gene expression changes in spinal cord from SOD1(G93A) Amyotrophic Lateral Sclerosis animal model.Molecular biological approaches to neurological disorders including knockout and transgenic mouse models.Insulin and glucagon share the same mechanism of neuroprotection in diabetic rats: role of glutamateMolecular and cellular pathways of neurodegeneration in motor neurone diseaseMiro1 deficiency in amyotrophic lateral sclerosis.Adaptive and maladaptive motor axonal sprouting in aging and motoneuron disease.Functional alterations of the ubiquitin-proteasome system in motor neurons of a mouse model of familial amyotrophic lateral sclerosisThe preclinical discovery of amyotrophic lateral sclerosis drugs.Elevated GFAP induces astrocyte dysfunction in caudal brain regions: A potential mechanism for hindbrain involved symptoms in type II Alexander disease.Rodent Models of Amyotrophic Lateral SclerosisRecent advances in amyotrophic lateral sclerosis research: perspectives for personalized clinical applicationThe role of glutamate transporters in neurodegenerative diseases and potential opportunities for intervention.Postactivation depression of the Ia EPSP in motoneurons is reduced in both the G127X SOD1 model of amyotrophic lateral sclerosis and in aged mice.Inter- and intracellular signaling in amyotrophic lateral sclerosis: role of p38 mitogen-activated protein kinase.Excitotoxicity and amyotrophic lateral sclerosis.Role of zinc in ALS.Mutant copper-zinc superoxide dismutase (SOD1) induces protein secretion pathway alterations and exosome release in astrocytes: implications for disease spreading and motor neuron pathology in amyotrophic lateral sclerosisThe four major N- and C-terminal splice variants of the excitatory amino acid transporter GLT-1 form cell surface homomeric and heteromeric assemblies.A high-fat jelly diet restores bioenergetic balance and extends lifespan in the presence of motor dysfunction and lumbar spinal cord motor neuron loss in TDP-43A315T mutant C57BL6/J mice.Homocysteine levels and amyotrophic lateral sclerosis: A possible link.Astrogliosis in amyotrophic lateral sclerosis: role and therapeutic potential of astrocytesNO orchestrates the loss of synaptic boutons from adult "sick" motoneurons: modeling a molecular mechanism.Review: The role of mitochondria in the pathogenesis of amyotrophic lateral sclerosis.Glutamate transporter EAAT2: regulation, function, and potential as a therapeutic target for neurological and psychiatric disease.Amyotrophic Lateral Sclerosis and Metabolomics: Clinical Implication and Therapeutic Approach.
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Transgenic SOD1 G93A mice develop reduced GLT-1 in spinal cord without alterations in cerebrospinal fluid glutamate levels.
description
2001 nî lūn-bûn
@nan
2001年の論文
@ja
2001年学术文章
@wuu
2001年学术文章
@zh
2001年学术文章
@zh-cn
2001年学术文章
@zh-hans
2001年学术文章
@zh-my
2001年学术文章
@zh-sg
2001年學術文章
@yue
2001年學術文章
@zh-hant
name
Transgenic SOD1 G93A mice deve ...... spinal fluid glutamate levels.
@en
Transgenic SOD1 G93A mice deve ...... spinal fluid glutamate levels.
@nl
type
label
Transgenic SOD1 G93A mice deve ...... spinal fluid glutamate levels.
@en
Transgenic SOD1 G93A mice deve ...... spinal fluid glutamate levels.
@nl
prefLabel
Transgenic SOD1 G93A mice deve ...... spinal fluid glutamate levels.
@en
Transgenic SOD1 G93A mice deve ...... spinal fluid glutamate levels.
@nl
P2093
P2860
P1476
Transgenic SOD1 G93A mice deve ...... spinal fluid glutamate levels.
@en
P2093
L Carvelli
M Tortarolo
N Calvaresi
S K Suchak
P2860
P304
P356
10.1046/J.1471-4159.2001.00572.X
P407
P577
2001-11-01T00:00:00Z