ReviewCurrent Alzheimer research2013
Impact of apolipoprotein E on Alzheimer's disease.
Review in Current Alzheimer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 97 citations in OpenAlex.
- Protective effect of apolipoprotein E epsilon 3 on sporadic Alzheimer's disease in the Chinese population: a meta-analysis.Scientific reports · 2022Pooled it
- Apolipoprotein E gene polymorphism and Alzheimer's disease in Chinese population: a meta-analysis.Scientific reports · 2014Pooled it
- Baseline predictors of neurophysiological response to combined physical and cognitive training in older adults with subjective cognitive decline.BMC geriatrics · 2026Trial
- Personalized whole-body modeling links gut microbiota to metabolic perturbations in Alzheimer's disease.Gut microbes · 2026Article
- In silico metabolic modelling links microbiome-derived metabolites to risk factors of Alzheimer's disease.Gut microbes reports · 2025Article
- Review
- Isolation of recombinant apolipoprotein E4 N-terminal domain by foam fractionation.Protein expression and purification · 2023Article
- Single-cell profiling of vascular endothelial cells reveals progressive organ-specific vulnerabilities during obesity.Nature metabolism · 2022Article
- Potential Mechanisms Underlying Resistance to Dementia in Non-Demented Individuals with Alzheimer's Disease Neuropathology.Journal of Alzheimer's disease : JAD · 2022Review
- Review
- Cognitive decline in amyotrophic lateral sclerosis: Neuropathological substrate and genetic determinants.Brain pathology (Zurich, Switzerland) · 2021Article
- Apolipoprotein E4 and meningeal lymphatics in Alzheimer disease: a conceptual framework.Molecular psychiatry · 2021Review
- Correlation between C9ORF72 mutation and neurodegenerative diseases: A comprehensive review of the literature.International journal of medical sciences · 2021Review
- Passive immunotherapies targeting Aβ and tau in Alzheimer's disease.Neurobiology of disease · 2020Review
- A Defined and Scalable Peptide-Based Platform for the Generation of Human Pluripotent Stem Cell-Derived Astrocytes.ACS biomaterials science & engineering · 2020Article
- BIG-TREE: Base-Edited Isogenic hPSC Line Generation Using a Transient Reporter for Editing Enrichment.Stem cell reports · 2020Article
- Clusterin as a Potential Biomarker of Obesity-Related Alzheimer's Disease Risk.Biomarker insights · 2020Review
- A transient reporter for editing enrichment (TREE) in human cells.Nucleic acids research · 2019Article
- Hidden Aggregation Hot-Spots on Human Apolipoprotein E: A Structural Study.International journal of molecular sciences · 2019Article
- Targeting Inflammatory Pathways in Alzheimer's Disease: A Focus on Natural Products and Phytomedicines.CNS drugs · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A key feature of Alzheimer's disease (AD) is deposition of extracellular amyloid plaque comprised chiefly of the amyloid β (Aβ) peptide. Studies of Aβ have shown that it may be catabolized by proteolysis or cleared from brain via members of the low-density lipoprotein receptor family. Alternatively, Aβ can undergo a conformational transition from α-helix to β-sheet, a conformer that displays a propensity to self-associate, oligomerize and form fibrils. Furthermore, β- sheet conformers catalyze conversion of other α-helical Aβ peptides to β-sheet, feeding the oligomer and fibril assembly process. A factor that influences the fate of Aβ in the extracellular space is apolipoprotein (apo) E. Polymorphism at position 112 or 158 in apoE give rise to three major isoforms. One isoform in particular, apoE4 (Arg at 112 and 158), has generated considerable interest since the discovery that it is the major genetic risk factor for development of late onset AD. Despite this striking correlation, the molecular mechanism underlying apoE4's association with AD remains unclear. A tertiary structural feature distinguishing apoE4 from apoE2 and apoE3, termed domain interaction, is postulated to affect the conformation and orientation of its' two independently folded domains. This feature has the potential to influence apoE4's interaction with Aβ, its sensitivity to proteolysis or its lipid accrual and receptor binding activities. Thus, domain interaction may constitute the principal molecular feature of apoE4 that predisposes carriers to late onset AD. By understanding the contribution of apoE4 to AD at the molecular level new therapeutic or prevention strategies will emerge.
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What OpenQuestion holds
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.