ArticlePloS one2012
In vivo human apolipoprotein E isoform fractional turnover rates in the CNS.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- ApoE lipoproteins in the central nervous system under homeostasis and role in Alzheimer's disease and related disorders.Molecular neurodegeneration · 2026Review
- Spatiotemporally resolved mapping of extracellular proteomes via in vivo-compatible TyroID.Nature communications · 2025Article
- Circulating apoE4 protein levels from dried blood spots predict cognitive function in a large population-based survey setting.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Modeling the Simultaneous Dynamics of Proteins in Blood Plasma and the Cerebrospinal Fluid in HumanJournal of proteome research · 2024Article
- Article
- Multi-peptide characterization of plasma neurofilament light chain in preclinical and mild Alzheimer's disease.Brain communications · 2024Article
- Plasma apolipoprotein E levels, isoform composition, and dimer profile in relation to plasma lipids in racially diverse patients with Alzheimer's disease and mild cognitive impairment.Alzheimer's research & therapy · 2023Article
- The role of ApoE-mediated microglial lipid metabolism in brain aging and disease.Immunometabolism (Cobham, Surrey) · 2023Review
- APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer's disease pathology and brain diseases.Molecular neurodegeneration · 2022Review
- Plasma apolipoprotein E levels in longitudinally followed patients with mild cognitive impairment and Alzheimer's disease.Alzheimer's research & therapy · 2022Article
- Impact of increased APP gene dose in Down syndrome and the Dp16 mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- ApoE Cascade Hypothesis in the pathogenesis of Alzheimer's disease and related dementias.Neuron · 2022Review
- Nogo receptor impairs the clearance of fibril amyloid-β by microglia and accelerates Alzheimer's-like disease progression.Aging cell · 2021Article
- Peripheral and central immune system crosstalk in Alzheimer disease - a research prospectus.Nature reviews. Neurology · 2021Review
- Using stable isotope labeling to advance our understanding of Alzheimer's disease etiology and pathology.Journal of neurochemistry · 2021Review
- Features of Lipid Metabolism in Humanized ApoE Knockin Rat Models.International journal of molecular sciences · 2021Article
- Plasma Apolipoprotein E3 and Glucose Levels Are Associated in APOE ɛ3/ɛ4 Carriers.Journal of Alzheimer's disease : JAD · 2021Article
- The Associations of Cerebrospinal Fluid ApoE and Biomarkers of Alzheimer's Disease: Exploring Interactions With Sex.Frontiers in neuroscience · 2021Article
- Apolipoprotein E Gene Polymorphism and Coronary Artery Disease Risk Among Patients in Northwest China.Pharmacogenomics and personalized medicine · 2021Article
- Therapeutic approaches targeting Apolipoprotein E function in Alzheimer's disease.Molecular neurodegeneration · 2020Review
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Apolipoprotein E (ApoE) is the strongest genetic risk factor for Alzheimer's disease and has been implicated in the risk for other neurological disorders. The three common ApoE isoforms (ApoE2, E3, and E4) each differ by a single amino acid, with ApoE4 increasing and ApoE2 decreasing the risk of Alzheimer's disease (AD). Both the isoform and amount of ApoE in the brain modulate AD pathology by altering the extent of amyloid beta (Aβ) peptide deposition. Therefore, quantifying ApoE isoform production and clearance rates may advance our understanding of the role of ApoE in health and disease. To measure the kinetics of ApoE in the central nervous system (CNS), we applied in vivo stable isotope labeling to quantify the fractional turnover rates of ApoE isoforms in 18 cognitively-normal adults and in ApoE3 and ApoE4 targeted-replacement mice. No isoform-specific differences in CNS ApoE3 and ApoE4 turnover rates were observed when measured in human CSF or mouse brain. However, CNS and peripheral ApoE isoform turnover rates differed substantially, which is consistent with previous reports and suggests that the pathways responsible for ApoE metabolism are different in the CNS and the periphery. We also demonstrate a slower turnover rate for CSF ApoE than that for amyloid beta, another molecule critically important in AD pathogenesis.
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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.