ArticleCellular and molecular neurobiology2009
Quantitative proteomic analysis of mitochondria in aging PS-1 transgenic mice.
Article in Cellular and molecular neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Start Me Up: How Can Surrounding Gangliosides Affect Sodium-Potassium ATPase Activity and Steer towards Pathological Ion Imbalance in Neurons?Biomedicines · 2022Review
- Effect of ginkgolide K on calcium channel activity in Alzheimer's disease.Experimental and therapeutic medicine · 2022Article
- Dynamic Mitochondrial Proteome Under Polyamines Treatment in Cardiac Aging.Frontiers in cell and developmental biology · 2022Article
- The role of melatonin in the treatment of type 2 diabetes mellitus and Alzheimer's disease.International journal of biological sciences · 2022Review
- Mitophagy alterations in Alzheimer's disease are associated with granulovacuolar degeneration and early tau pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020Article
- Proteomic analysis links alterations of bioenergetics, mitochondria-ER interactions and proteostasis in hippocampal astrocytes from 3xTg-AD mice.Cell death & disease · 2020Article
- Mitochondrial dysfunction in Alzheimer's disease: Role in pathogenesis and novel therapeutic opportunities.British journal of pharmacology · 2019Review
- Discovery of Age-Related Protein Folding Stability Differences in the Mouse Brain Proteome.Journal of proteome research · 2016Article
- Molecular and biochemical trajectories from diabetes to Alzheimer's disease: A critical appraisal.World journal of diabetes · 2015Review
- Mitochondrial toxic effects of Aβ through mitofusins in the early pathogenesis of Alzheimer's disease.Molecular neurobiology · 2014Article
- Biomarkers in Alzheimer's disease analysis by mass spectrometry-based proteomics.International journal of molecular sciences · 2014Review
- Recent advances in quantitative neuroproteomics.Methods (San Diego, Calif.) · 2013Review
- From mitochondrial dysfunction to amyloid beta formation: novel insights into the pathogenesis of Alzheimer's disease.Molecular neurobiology · 2012Review
- Mitochondrial DNA deletions and differential mitochondrial DNA content in Rhesus monkeys: implications for aging.Biochimica et biophysica acta · 2012Article
- Presenilin transgenic mice as models of Alzheimer's disease.Brain structure & function · 2010Review
- Capillary endothelial Na(+), K(+), ATPase transporter homeostasis and a new theory for migraine pathophysiology.Headache · 2010Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Accumulating evidence suggests mitochondrial alterations are intimately associated with the pathogenesis of Alzheimer's disease (AD). In order to determine if mutations of presenilin-1 (PS-1) affect levels of mitochondrial proteins at different ages we enriched mitochondrial fractions from 3-, 6-, 12-month-old knock-in mice expressing the M146V PS-1 mutation and identified, and quantified proteins using cleavable isotope-coded affinity tag labeling and two-dimensional liquid chromatography/tandem mass spectrometry (2D-LC/MS/MS). Using this approach, 165 non-redundant proteins were identified with 80 of them present in all three age groups. Specifically, at young ages (3 and 6 months), Na(+)/K(+) ATPase and several signal transduction proteins exhibited elevated levels, but dropped dramatically at 12 months. In contrast, components of the oxidative phosporylation pathway (OXPHOS), the mitochondrial permeability transition pore (MPTP), and energy metabolism proteins remained unchanged at 3 months but significantly increased with age. We propose that alterations in calcium homeostasis induced by the PS-1 mutation have a major impact in young animals by inhibiting the function of relevant proteins and inducing compensatory changes. However, in older mice combination of the PS-1 mutation and accumulated oxidative damage results in a functional suppression of OXPHOS and MPTP proteins requiring a compensatory increase in expression levels. In contrast, signal transduction proteins showed decreased levels due to a break down in the compensatory mechanisms. The dysfunction of Na(+)/K(+) ATPase and signal transduction proteins may induce impaired cognition and memory before neurodegeneration occurs.
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