ArticlePloS one2013
Mass spectrometry quantification revealed accumulation of C-terminal fragment of apolipoprotein E in the Alzheimer's frontal cortex.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 16 citations in OpenAlex.
- Mass Spectrometry-Based Analysis of Lipid Involvement in Alzheimer's Disease Pathology-A Review.Metabolites · 2022Review
- Are apolipoprotein E fragments a promising new therapeutic target for Alzheimer's disease?Therapeutic advances in chronic disease · 2022Review
- ApoE-fragment/Aβ heteromers in the brain of patients with Alzheimer's disease.Scientific reports · 2019Article
- Vascular proteomics in metabolic and cardiovascular diseases.Journal of internal medicine · 2016Review
- The ability of apolipoprotein E fragments to promote intraneuronal accumulation of amyloid beta peptide 42 is both isoform and size-specific.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Polymorphic variation in the apolipoprotein E (apoE) gene is the major genetic susceptibility factor for late-onset Alzheimer's disease (AD) and likely contributes to neuropathology through various pathways. It is also recognized that apoE undergoes proteolytic cleavage in the brain and the resultant apoE fragments likely have a variety of bioactive properties that regulate neuronal signaling and may promote neurodegeneration. ApoE fragmentation in the human brain has been intensively studied using different immunochemical methods, but has never been analyzed in a quantitative manner to establish preferably accumulated fragments. Here we report quantification using multiple reaction monitoring mass spectrometry (MRM MS) with (15)N-labeled full-length apoE4 as an internal standard. Measurements were performed on frontal cortex from control and severe AD donors. Our data point to a preferable accumulation of C-terminal apoE fragment in the insoluble fraction of tissue homogenate in the severe AD group versus the control group. Further insight into the biological consequences of this accumulation may lead to a better understanding of the basic mechanism of AD pathology.
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Registered trials
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