Individual Amino Acid Supplementation Can Improve Energy Metabolism and Decrease ROS Production in Neuronal Cells Overexpressing Alpha-Synuclein.

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Individual Amino Acid Supplementation Can Improve Energy Metabolism and Decrease ROS Production in Neuronal Cells Overexpressing Alpha-Synuclein.

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http://www.wikidata.org/entity/Q46349223

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2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年學術文章

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2017年學術文章

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name

Individual Amino Acid Suppleme ...... verexpressing Alpha-Synuclein.

@en

Individual Amino Acid Suppleme ...... verexpressing Alpha-Synuclein.

@nl

type

Item

label

Individual Amino Acid Suppleme ...... verexpressing Alpha-Synuclein.

@en

Individual Amino Acid Suppleme ...... verexpressing Alpha-Synuclein.

@nl

prefLabel

Individual Amino Acid Suppleme ...... verexpressing Alpha-Synuclein.

@en

Individual Amino Acid Suppleme ...... verexpressing Alpha-Synuclein.

@nl

P1476

Individual Amino Acid Suppleme ...... verexpressing Alpha-Synuclein.

@en

P2093

Christian Reynes

http://www.w3.org/2001/XMLSchema#string

Dale Chaput

http://www.w3.org/2001/XMLSchema#string

Daniel C Lee

http://www.w3.org/2001/XMLSchema#string

Devon Placides

http://www.w3.org/2001/XMLSchema#string

Eni Cvitkovic

http://www.w3.org/2001/XMLSchema#string

Ernide Frederic

http://www.w3.org/2001/XMLSchema#string

Hamed Mirzaei

http://www.w3.org/2001/XMLSchema#string

Henry Gong

http://www.w3.org/2001/XMLSchema#string

Jeddidiah W D Griffin

http://www.w3.org/2001/XMLSchema#string

Josean Cruz

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P2860

Mutant and wild-type alpha-synuclein interact with mitochondrial cytochrome C oxidase

Alpha-synuclein acts in the nucleus to inhibit histone acetylation and promote neurotoxicity

α-Synuclein occurs physiologically as a helically folded tetramer that resists aggregation

Imputation of sequence variants for identification of genetic risks for Parkinson's disease: a meta-analysis of genome-wide association studies

MAO-B elevation in mouse brain astrocytes results in Parkinson's pathology

Therapeutic applications of selective and non-selective inhibitors of monoamine oxidase A and B that do not cause significant tyramine potentiation

Platelet monoamine oxidase B and plasma beta-phenylethylamine in Parkinson's disease

Selective binding of nuclear alpha-synuclein to the PGC1alpha promoter under conditions of oxidative stress may contribute to losses in mitochondrial function: implications for Parkinson's disease

BDNF increases rat brain mitochondrial respiratory coupling at complex I, but not complex II

The new mutation, E46K, of alpha-synuclein causes Parkinson and Lewy body dementia

P2888

s12017-017-8448-8

P304

322-344

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P31

scholarly article

P356

10.1007/S12017-017-8448-8

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P433

2-3

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P478

http://www.w3.org/2001/XMLSchema#string

P50

Patrick C Bradshaw

P577

2017-06-15T00:00:00Z

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P698

28620826

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P921

Synuclein

overexpression