Mitochondrial respiratory inhibition and oxidative stress elevate beta-secretase (BACE1) proteins and activity in vivo in the rat retina. (Q48206372)

9 February 2018

title

Mitochondrial respiratory inhibition and oxidative stress elevate beta-secretase (BACE1) proteins and activity in vivo in the rat retina. (English)

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9 February 2018

Huaibin Cai

2

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author name string

Kun Xiong

1

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9 February 2018

Xue-Gang Luo

3

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9 February 2018

Robert G Struble

4

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9 February 2018

Richard W Clough

5

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9 February 2018

Xiao-Xin Yan

6

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9 February 2018

publication date

12 April 2007

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9 February 2018

Experimental Brain Research

published in

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9 February 2018

volume

181

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9 February 2018

page(s)

435-446

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9 February 2018

issue

3

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9 February 2018

https://scigraph.springernature.com/pub.10.1007/s00221-007-0943-y

exact match

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cites work

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Proteolytic processing of the amyloid-beta protein precursor of Alzheimer's disease

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Oxidative stress increases expression and activity of BACE in NT2 neurons

21 January 2018

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Iron, neuroinflammation, and Alzheimer's disease

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Thioflavine T interaction with synthetic Alzheimer's disease beta-amyloid peptides: detection of amyloid aggregation in solution

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Increased beta-secretase activity and expression in rats following transient cerebral ischemia

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Mitochondrial respiratory chain activity in the human brain as a function of age

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Correlations between apolipoprotein E epsilon4 gene dose and brain-imaging measurements of regional hypometabolism

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Ageing and neuronal vulnerability

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Toward a comprehensive theory for Alzheimer's disease. Hypothesis: Alzheimer's disease is caused by the cerebral accumulation and cytotoxicity of amyloid beta-protein.

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Elevated beta-secretase expression and enzymatic activity detected in sporadic Alzheimer disease

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Mitoenergetic failure in Alzheimer disease

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BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions.

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Beta-site APP cleaving enzyme 1 (BACE1) is increased in remaining neurons in Alzheimer's disease brains

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A "mitochondrial cascade hypothesis" for sporadic Alzheimer's disease

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RAC1 inhibition targets amyloid precursor protein processing by gamma-secretase and decreases Abeta production in vitro and in vivo.

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Amyloid beta peptide causes chronic glial cell activation and neuro-degeneration after intravitreal injection

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Amyloid precursor protein-mediated free radicals and oxidative damage: implications for the development and progression of Alzheimer's disease

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Brain glucose metabolism in the early and specific diagnosis of Alzheimer's disease. FDG-PET studies in MCI and AD.

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Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease

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Oxidative stress in neurodegeneration: cause or consequence?

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Maturation and endosomal targeting of beta-site amyloid precursor protein-cleaving enzyme. The Alzheimer's disease beta-secretase

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Cytochrome oxidase in Alzheimer's disease: biochemical, histochemical, and immunohistochemical analyses of the visual and other systems.

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Energy hypometabolism in posterior cingulate cortex of Alzheimer's patients: superficial laminar cytochrome oxidase associated with disease duration.

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12 December 2020

Experimental traumatic brain injury in rats stimulates the expression, production and activity of Alzheimer's disease beta-secretase (BACE-1).

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12 December 2020

Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression

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12 December 2020

Chronic in vivo sodium azide infusion induces selective and stable inhibition of cytochrome c oxidase.

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12 December 2020

alpha- and beta-secretase: profound changes in Alzheimer's disease.

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12 December 2020

Oxidative stress potentiates BACE1 gene expression and Abeta generation

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12 December 2020

Energy inhibition elevates beta-secretase levels and activity and is potentially amyloidogenic in APP transgenic mice: possible early events in Alzheimer's disease pathogenesis.

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Binding sites of gamma-secretase inhibitors in rodent brain: distribution, postnatal development, and effect of deafferentation.

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Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease

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Alzheimer's disease: genes, proteins, and therapy

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Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain

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Amyloid beta peptide load is correlated with increased beta-secretase activity in sporadic Alzheimer's disease patients

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beta-Secretase expression in normal and functionally deprived rat olfactory bulbs: inverse correlation with oxidative metabolic activity.

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Fluid ‘rope trick’ investigated

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The various aggregation states of beta-amyloid 1-42 mediate different effects on oxidative stress, neurodegeneration, and BACE-1 expression

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Mechanism of toxicity in rotenone models of Parkinson's disease

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Oxidative stress and redox-active iron in Alzheimer's disease

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3-nitropropionic acid is a suicide inhibitor of mitochondrial respiration that, upon oxidation by complex II, forms a covalent adduct with a catalytic base arginine in the active site of the enzyme

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10.1007/S00221-007-0943-Y

Identifiers

DOI

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9 February 2018

PubMed ID

17429617

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9 February 2018