Treatment with Trehalose Prevents Behavioral and Neurochemical Deficits Produced in an AAV α-Synuclein Rat Model of Parkinson's Disease (Q41740088)

8 October 2017

Treatment with Trehalose Prevents Behavioral and Neurochemical Deficits Produced in an AAV α-Synuclein Rat Model of Parkinson's Disease (English)

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8 October 2017

alpha,alpha-trehalose

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6

Jonathan M Brotchie

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8 October 2017

Qing He

1

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8 October 2017

James B Koprich

2

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8 October 2017

Ying Wang

3

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8 October 2017

Wen-bo Yu

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8 October 2017

Bao-guo Xiao

5

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8 October 2017

Jian Wang

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8 October 2017

language of work or name

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14 May 2015

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8 October 2017

Molecular Neurobiology

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8 October 2017

53

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8 October 2017

4

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8 October 2017

2258-2268

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https://scigraph.springernature.com/pub.10.1007/s12035-015-9173-7

8 October 2017

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alpha-Synuclein locus triplication causes Parkinson's disease

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The Parkinson disease-associated A30P mutation stabilizes alpha-synuclein against proteasomal degradation triggered by heme oxygenase-1 over-expression in human neuroblastoma cells.

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Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease

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Trehalose: a review of properties, history of use and human tolerance, and results of multiple safety studies

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Can trehalose prevent neurodegeneration? Insights from experimental studies

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Trehalose, a novel mTOR-independent autophagy enhancer, accelerates the clearance of mutant huntingtin and alpha-synuclein.

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Human platelets loaded with trehalose survive freeze-drying

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Progressive neurodegeneration or endogenous compensation in an animal model of Parkinson's disease produced by decreasing doses of alpha-synuclein

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Expression of human A53T alpha-synuclein in the rat substantia nigra using a novel AAV1/2 vector produces a rapidly evolving pathology with protein aggregation, dystrophic neurite architecture and nigrostriatal degeneration with potential to model t

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LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing

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Small molecules enhance autophagy and reduce toxicity in Huntington's disease models.

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The accumulation of neurotoxic proteins, induced by proteasome inhibition, is reverted by trehalose, an enhancer of autophagy, in human neuroblastoma cells

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Trehalose alleviates polyglutamine-mediated pathology in a mouse model of Huntington disease

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Stimulation of autophagy reduces neurodegeneration in a mouse model of human tauopathy

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Effect of trehalose on PC12 cells overexpressing wild-type or A53T mutant α-synuclein

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Neuroprotective effect of the chemical chaperone, trehalose in a chronic MPTP-induced Parkinson's disease mouse model

21 January 2018

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Dynamic changes in presynaptic and axonal transport proteins combined with striatal neuroinflammation precede dopaminergic neuronal loss in a rat model of AAV alpha-synucleinopathy.

21 January 2018

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Trehalose: a biophysics approach to modulate the inflammatory response during endotoxic shock.

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Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage

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Acute administration of fluoxetine normalizes rapid eye movement sleep abnormality, but not depressive behaviors in olfactory bulbectomized rats.

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Metal-catalyzed oxidation of alpha-synuclein: helping to define the relationship between oligomers, protofibrils, and filaments

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12 December 2020

Therapeutic efficacy of trehalose eye drops for treatment of murine dry eye induced by an intelligently controlled environmental system

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12 December 2020

Aggregation of ?-synuclein in the pathogenesis of Parkinson?s disease

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12 December 2020

The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice

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12 December 2020

Effect of trehalose on protein structure

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12 December 2020

Trehalose inhibits fibrillation of A53T mutant alpha-synuclein and disaggregates existing fibrils

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12 December 2020

10.1007/S12035-015-9173-7

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DOI

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Dimensions Publication ID

8 October 2017

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