Cytochrome c oxidase deficiency in neurons decreases both oxidative stress and amyloid formation in a mouse model of Alzheimer's disease - Wikidata - wikimedia - TriplyDB

Cytochrome c oxidase deficiency in neurons decreases both oxidative stress and amyloid formation in a mouse model of Alzheimer's disease

Cytochrome c oxidase deficiency in neurons decreases both oxidative stress and amyloid formation in a mouse model of Alzheimer's disease

http://www.wikidata.org/entity/Q30443526

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Mitochondrial genome changes and neurodegenerative diseases The GRACILE mutation introduced into Bcs1l causes postnatal complex III deficiency: a viable mouse model for mitochondrial hepatopathy Partial complex I deficiency due to the CNS conditional ablation of Ndufa5 results in a mild chronic encephalopathy but no increase in oxidative damage.A defect in the mitochondrial complex III, but not complex IV, triggers early ROS-dependent damage in defined brain regions.Reduced IGF-1 signaling delays age-associated proteotoxicity in mice Metabolite profiles reveal energy failure and impaired beta-oxidation in liver of mice with complex III deficiency due to a BCS1L mutation.Mitochondrial DNA damage in a mouse model of Alzheimer's disease decreases amyloid beta plaque formation Docking Studies and Biological Evaluation of a Potential β-Secretase Inhibitor of 3-Hydroxyhericenone F from Hericium erinaceus.Aging: Dial M for Mitochondria Xanthoceraside ameliorates mitochondrial dysfunction contributing to the improvement of learning and memory impairment in mice with intracerebroventricular injection of aβ1-42.Amelioration of Cognitive Dysfunction in APP/PS1 Double Transgenic Mice by Long-Term Treatment of 4-O-Methylhonokiol.Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer's disease.The Alzheimer's disease mitochondrial cascade hypothesis Preclinical Alzheimer disease: brain oxidative stress, Abeta peptide and proteomics.A synergistic dysfunction of mitochondrial fission/fusion dynamics and mitophagy in Alzheimer's disease.Age-related neuronal degeneration: complementary roles of nucleotide excision repair and transcription-coupled repair in preventing neuropathology Catalytic antioxidants and neurodegeneration Vascular and metabolic dysfunction in Alzheimer's disease: a review.Amyloid-β peptide binds to cytochrome C oxidase subunit 1.Meclizine is neuroprotective in models of Huntington's disease.CD45 deficiency drives amyloid-β peptide oligomers and neuronal loss in Alzheimer's disease mice Placental genome and maternal-placental genetic interactions: a genome-wide and candidate gene association study of placental abruption Large-scale in silico modeling of metabolic interactions between cell types in the human brain.Aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction in Alzheimer's disease: implications for early intervention and therapeutics.Cardiac deficiency of single cytochrome oxidase assembly factor scox induces p53-dependent apoptosis in a Drosophila cardiomyopathy model Mitochondria and cell bioenergetics: increasingly recognized components and a possible etiologic cause of Alzheimer's disease.Mitochondrion-derived reactive oxygen species lead to enhanced amyloid beta formation.Role of mitochondrial homeostasis and dynamics in Alzheimer's disease.Enhanced Transcriptional Activity and Mitochondrial Localization of STAT3 Co-induce Axon Regrowth in the Adult Central Nervous System.Investigation of cytocrom c oxidase gene subunits expression on the Multiple sclerosis Mouse models of oxidative phosphorylation defects: powerful tools to study the pathobiology of mitochondrial diseases.Mouse models of oxidative phosphorylation dysfunction and disease The mitochondrial impairment, oxidative stress and neurodegeneration connection: reality or just an attractive hypothesis?Mitochondria in neuroplasticity and neurological disorders.The Alzheimer's disease mitochondrial cascade hypothesis: an update The pathophysiology of mitochondrial disease as modeled in the mouse.Impaired mitochondrial energy production and ABC transporter function-A crucial interconnection in dementing proteopathies of the brain.Pharmacological approaches to restore mitochondrial function.The Alzheimer's disease mitochondrial cascade hypothesis: progress and perspectives.Turn up the power - pharmacological activation of mitochondrial biogenesis in mouse models.

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Cytochrome c oxidase deficiency in neurons decreases both oxidative stress and amyloid formation in a mouse model of Alzheimer's disease

http://www.wikidata.org/entity/Q30443526

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2007 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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Cytochrome c oxidase deficienc ...... e model of Alzheimer's disease

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Carlos T Moraes

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Francisca Diaz

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Sofia Garcia

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P2860

Cytochrome c oxidase and mitochondrial F1F0-ATPase (ATP synthase) activities in platelets and brain from patients with Alzheimer's disease

Amyloid-beta peptide binds with heme to form a peroxidase: relationship to the cytopathologies of Alzheimer's disease

Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency

Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases

Mice lacking COX10 in skeletal muscle recapitulate the phenotype of progressive mitochondrial myopathies associated with cytochrome c oxidase deficiency.

Cytochrome c oxidase is required for the assembly/stability of respiratory complex I in mouse fibroblasts

A systematic RNAi screen identifies a critical role for mitochondria in C. elegans longevity

Natural oligomers of the amyloid-beta protein specifically disrupt cognitive function

Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging

High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease

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