ArticleJournal of Alzheimer's disease : JAD2010
Quantitative changes in the mitochondrial proteome from subjects with mild cognitive impairment, early stage, and late stage Alzheimer's disease.
Article in Journal of Alzheimer's disease : JAD, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 39 citations in OpenAlex.
- Restoration of Enzymatic Activity of Energy-Related Proteins in Rats with Traumatic Brain Injury Following Administration of Gamma-Glutamylcysteine Ethyl Ester.Brain sciences · 2025Article
- Hexokinase as a Central Hub in Neurodegeneration: From Metabolic Dysfunction to Therapeutic Innovation.Aging and disease · 2025Review
- Frontal cortex pyramidal neuron expression profiles differentiate the prodromal stage from progressive degeneration across the Alzheimer's disease spectrum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Copper metabolism-related Genes in entorhinal cortex for Alzheimer's disease.Scientific reports · 2023Article
- A tau fragment links depressive-like behaviors and cognitive declines in Alzheimer's disease mouse models through attenuating mitochondrial function.Frontiers in aging neuroscience · 2023Article
- Mechanistic perspectives on differential mitochondrial-based neuroprotective effects of several carnitine forms in Alzheimer's disease in vitro model.Archives of toxicology · 2021Article
- Oral administration of D-galactose increases brain tricarboxylic acid cycle enzymes activities in Wistar rats.Metabolic brain disease · 2021Article
- Mitochondrial Permeability Transition: A Pore Intertwines Brain Aging and Alzheimer's Disease.Cells · 2021Review
- Dynamic changes in the brain protein interaction network correlates with progression of Aβ42 pathology in Drosophila.Scientific reports · 2020Article
- Alcohol drinking exacerbates neural and behavioral pathology in the 3xTg-AD mouse model of Alzheimer's disease.International review of neurobiology · 2019Review
- Maternal imprinting on cognition markers of wild type and transgenic Alzheimer's disease model mice.Scientific reports · 2018Article
- Altered brain high-energy phosphate metabolism in mild Alzheimer's disease: A 3-dimensionalNeuroImage. Clinical · 2018Article
- Neurodegeneration and Alzheimer's disease (AD). What Can Proteomics Tell Us About the Alzheimer's Brain?Molecular & cellular proteomics : MCP · 2016Review
- Clinical implications from proteomic studies in neurodegenerative diseases: lessons from mitochondrial proteins.Expert review of proteomics · 2016Review
- Deep Phosphoproteomic Measurements Pinpointing Drug Induced Protective Mechanisms in Neuronal Cells.Frontiers in physiology · 2016Article
- Glutamate and GABA-metabolizing enzymes in post-mortem cerebellum in Alzheimer's disease: phosphate-activated glutaminase and glutamic acid decarboxylase.Cerebellum (London, England) · 2014Article
- Brain gene expression patterns differentiate mild cognitive impairment from normal aged and Alzheimer's disease.Neurobiology of aging · 2014Article
- Brain site-specific proteome changes in aging-related dementia.Experimental & molecular medicine · 2013Article
- A mitochondrial etiology of Alzheimer and Parkinson disease.Biochimica et biophysica acta · 2012Review
- Analysis of a membrane-enriched proteome from postmortem human brain tissue in Alzheimer's disease.Proteomics. Clinical applications · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The major barrier to treating or preventing Alzheimer's disease (AD) is its unknown etiology and pathogenesis. Although increasing evidence supports a role for mitochondrial dysfunction in the pathogenesis of AD, there have been few studies that simultaneously evaluate changes in multiple mitochondrial proteins. To evaluate changes in sites of potentially interacting mitochondrial proteins, we applied 2-dimensional liquid chromatography coupled with tandem mass spectrometry and the isotope coded affinity tag method to identify and quantify proteins in mitochondrial enriched fractions isolated from short postmortem interval temporal pole specimens from subjects with mild cognitive impairment (4 subjects pooled), early AD (4 subjects pooled), late-stage AD (8 subjects pooled) and age-matched normal control (7 subjects pooled) subjects. A total of 112 unique, non-redundant proteins were identified and quantified in common to all three stages of disease progression. Overall, patterns of protein change suggest activation of mitochondrial pathways that include proteins responsible for transport and utilization of ATP. These proteins include adenine nucleotide translocase, voltage dependent anion channels, hexokinase, and creatine kinase. Comparison of protein changes throughout the progression of AD suggests the most pronounced changes occur in early AD mitochondria.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.