Decline in mitochondrial bioenergetics and shift to ketogenic profile in brain during reproductive senescence - Wikidata - wikimedia - TriplyDB

Decline in mitochondrial bioenergetics and shift to ketogenic profile in brain during reproductive senescence

Decline in mitochondrial bioenergetics and shift to ketogenic profile in brain during reproductive senescence

http://www.wikidata.org/entity/Q35433892

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Shift in brain metabolism in late onset Alzheimer's disease: implications for biomarkers and therapeutic interventions Glucocorticoid-dependent hippocampal transcriptome in male rats: pathway-specific alterations with aging 2-Deoxy-D-glucose treatment induces ketogenesis, sustains mitochondrial function, and reduces pathology in female mouse model of Alzheimer's disease Ketogenic diet improves motor performance but not cognition in two mouse models of Alzheimer's pathology A theory of eu-estrogenemia: a unifying concept.Premature menopause and risk of neurological disease: basic mechanisms and clinical implications Continuous versus cyclic progesterone exposure differentially regulates hippocampal gene expression and functional profiles Vascular and metabolic dysfunction in Alzheimer's disease: a review.A mitochondrial etiology of Alzheimer and Parkinson disease Targeting mitochondrial bioenergetics for Alzheimer's prevention and treatment.Ovariectomy induces a shift in fuel availability and metabolism in the hippocampus of the female transgenic model of familial Alzheimer's.Hippocampal responsiveness to 17β-estradiol and equol after long-term ovariectomy: implication for a therapeutic window of opportunity.Mitochondrial oxygen consumption deficits in skeletal muscle isolated from an Alzheimer's disease-relevant murine model Ovarian hormone loss induces bioenergetic deficits and mitochondrial β-amyloid Estrogen protection against mitochondrial toxin-induced cell death in hippocampal neurons: antagonism by progesterone.The perimenopausal aging transition in the female rat brain: decline in bioenergetic systems and synaptic plasticity Reporting of sex as a variable in cardiovascular studies using cultured cells Estrogen neuroprotection and the critical period hypothesis.Inhibition of amyloid-beta (Abeta) peptide-binding alcohol dehydrogenase-Abeta interaction reduces Abeta accumulation and improves mitochondrial function in a mouse model of Alzheimer's disease Minireview: translational animal models of human menopause: challenges and emerging opportunities.Impact of Type 2 Diabetes and Postmenopausal Hormone Therapy on Incidence of Cognitive Impairment in Older Women White Matter Lipids as a Ketogenic Fuel Supply in Aging Female Brain: Implications for Alzheimer's Disease.Prolonged ovarian hormone deprivation alters the effects of 17β-estradiol on microRNA expression in the aged female rat hypothalamus.Age, APOE and sex: Triad of risk of Alzheimer's disease.STX, a Novel Membrane Estrogen Receptor Ligand, Protects Against Amyloid-β Toxicity.Early decline in glucose transport and metabolism precedes shift to ketogenic system in female aging and Alzheimer's mouse brain: implication for bioenergetic intervention.Hippocampal calcium dysregulation at the nexus of diabetes and brain aging.Mitochondrial energy metabolism and redox signaling in brain aging and neurodegeneration Estrogen regulation of mitochondrial bioenergetics: implications for prevention of Alzheimer's disease.The pyruvate dehydrogenase complex as a therapeutic target for age-related diseases.Effects of polyphenols on brain ageing and Alzheimer's disease: focus on mitochondria.Perimenopause as a neurological transition state.Estrogen Signaling as a Therapeutic Target in Neurodevelopmental Disorders.Brain aging and neurodegeneration: from a mitochondrial point of view.Proteomic differences in brain vessels of Alzheimer's disease mice: Normalization by PPARγ agonist pioglitazone.Insulin Resistance and Alzheimer's Disease: Bioenergetic Linkages.Role of Sex Hormones on Brain Mitochondrial Function, with Special Reference to Aging and Neurodegenerative Diseases.Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair.Metabolomic investigation of systemic manifestations associated with Alzheimer's disease in the APP/PS1 transgenic mouse model.High throughput multiorgan metabolomics in the APP/PS1 mouse model of Alzheimer's disease.

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P2860

Decline in mitochondrial bioenergetics and shift to ketogenic profile in brain during reproductive senescence

http://www.wikidata.org/entity/Q35433892

description

2010 nî lūn-bûn

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2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年学术文章

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2010年学术文章

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2010年學術文章

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name

Decline in mitochondrial bioen ...... during reproductive senescence

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Decline in mitochondrial bioen ...... during reproductive senescence

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type

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Decline in mitochondrial bioen ...... during reproductive senescence

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Decline in mitochondrial bioen ...... during reproductive senescence

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Decline in mitochondrial bioen ...... during reproductive senescence

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Biochimica et Biophysica Acta

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Decline in mitochondrial bioen ...... during reproductive senescence

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Enrique Cadenas

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Jia Yao

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Roberta Diaz Brinton

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Ryan T Hamilton

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P2860

Hypometabolism as a therapeutic target in Alzheimer's disease

Hormone replacement therapy to maintain cognitive function in women with dementia

Pathways towards and away from Alzheimer's disease

Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia

A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: a dawn for evolutionary medicine

Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Abeta and synaptic dysfunction

Linking brain imaging and genomics in the study of Alzheimer's disease and aging.

Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set.

Inherent abnormalities in energy metabolism in Alzheimer disease. Interaction with cerebrovascular compromise.

The neurodegenerative mitochondriopathies.

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