Decreased brain protein levels of cytochrome oxidase subunits in Alzheimer's disease and in hereditary spinocerebellar ataxia disorders: a nonspecific change? - Wikidata - awgldk - TriplyDB

Decreased brain protein levels of cytochrome oxidase subunits in Alzheimer's disease and in hereditary spinocerebellar ataxia disorders: a nonspecific change?

Decreased brain protein levels of cytochrome oxidase subunits in Alzheimer's disease and in hereditary spinocerebellar ataxia disorders: a nonspecific change?

http://www.wikidata.org/entity/Q34490690

about

Mitochondrial abnormalities in Alzheimer's disease: possible targets for therapeutic intervention Triad of Risk for Late Onset Alzheimer's: Mitochondrial Haplotype, APOE Genotype and Chromosomal Sex A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: a dawn for evolutionary medicine Mitochondrial DNA sequence associations with dementia and amyloid-β in elderly African Americans The effect of 5-aminolevulinic acid on cytochrome c oxidase activity in mouse liver.Inherent abnormalities in energy metabolism in Alzheimer disease. Interaction with cerebrovascular compromise.The neurodegenerative mitochondriopathies.Beta-amyloid mediated nitration of manganese superoxide dismutase: implication for oxidative stress in a APPNLH/NLH X PS-1P264L/P264L double knock-in mouse model of Alzheimer's disease.Cerebrometabolic abnormalities in Alzheimer's disease.Mitochondria and cell bioenergetics: increasingly recognized components and a possible etiologic cause of Alzheimer's disease.Amyloid-beta-induced mitochondrial dysfunction.Alzheimer's brains harbor somatic mtDNA control-region mutations that suppress mitochondrial transcription and replication The Alzheimer's disease mitochondrial cascade hypothesis: an update Mitochondrial Dysfunction and Synaptic Transmission Failure in Alzheimer's Disease.Cumulative effects of the ApoE genotype and gender on the synaptic proteome and oxidative stress in the mouse brain.Amyloid precursor protein drives down-regulation of mitochondrial oxidative phosphorylation independent of amyloid beta.Mitochondrial Translocase of the Outer Membrane Alterations May Underlie Dysfunctional Oxidative Phosphorylation in Alzheimer's Disease.Facilitation of brain mitochondrial activity by 5-aminolevulinic acid in a mouse model of Alzheimer's disease.Towards an Integrative Understanding of tRNA Aminoacylation-Diet-Host-Gut Microbiome Interactions in Neurodegeneration.

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P2860

Decreased brain protein levels of cytochrome oxidase subunits in Alzheimer's disease and in hereditary spinocerebellar ataxia disorders: a nonspecific change?

http://www.wikidata.org/entity/Q34490690

description

1999 nî lūn-bûn

@nan

1999 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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1999 թվականի փետրվարին հրատարակված գիտական հոդված

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1999年の論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年论文

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name

Decreased brain protein levels ...... sorders: a nonspecific change?

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Decreased brain protein levels ...... sorders: a nonspecific change?

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Decreased brain protein levels ...... sorders: a nonspecific change?

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Decreased brain protein levels ...... sorders: a nonspecific change?

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Decreased brain protein levels ...... sorders: a nonspecific change?

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Decreased brain protein levels ...... sorders: a nonspecific change?

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J.1471-4159.1999.0720700.X

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Journal of Neurochemistry

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Decreased brain protein levels ...... sorders: a nonspecific change?

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F Mastrogiacomo

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J Lamarche

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L DiStefano

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L J Chang

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M Guttman

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M Pandolfo

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S Dozić

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S J Kish

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Y Furukawa

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P2860

Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion

The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer's disease

Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease

Cytochrome c oxidase in Alzheimer's disease brain: purification and characterization.

Cybrids in Alzheimer's disease: a cellular model of the disease?

Evidence that two reports of mtDNA cytochrome c oxidase "mutations" in Alzheimer's disease are based on nDNA pseudogenes of recent evolutionary origin.

Anatomic and disease specificity of NADH CoQ1 reductase (complex I) deficiency in Parkinson's disease.

Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1.

Cytochrome oxidase: an endogenous metabolic marker for neuronal activity.

Apparent mtDNA heteroplasmy in Alzheimer's disease patients and in normals due to PCR amplification of nucleus-embedded mtDNA pseudogenes

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700-707

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Alzheimer's disease