ReviewMolecular neurobiology2018
Transcriptional Effects of ApoE4: Relevance to Alzheimer's Disease.
Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis 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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Rationale for a Multi-Factorial Approach for the Reversal of Cognitive Decline in Alzheimer's Disease and MCI: A Review.International journal of molecular sciences · 2023Pooled it
- Increased alcohol drinking and seizure susceptibility in female humanized ApoE4 knockin rats.Physiology & behavior · 2026Article
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- Harmony in Motion: The Role of Exercise in Orchestrating Neuroprotection for Individuals with Alzheimer's Disease and Diabetes Examined from a Psychological Perspective.Current pharmaceutical biotechnology · 2026Review
- Short-Term Changes in Depressive Symptoms Among Patients with Alzheimer's Disease Following a Precision Medicine Intervention.Brain sciences · 2025Article
- Pluripotent Cells Expressing APOE4 Exhibit a Pronounced Pro-Apoptotic Phenotype Accompanied by Markers of Hyperinflammation and a Blunted NF-κB Response.International journal of molecular sciences · 2025Article
- Meningeal lymphatic drainage: novel insights into central nervous system disease.Signal transduction and targeted therapy · 2025Review
- The role ofFrontiers in neuroscience · 2025Review
- Astrocytes in functional recovery following central nervous system injuries.The Journal of physiology · 2024Review
- Estradiol improves behavior in FAD transgenic mice that expressFrontiers in endocrinology · 2024Article
- Curcumin, inflammation, and neurological disorders: How are they linked?Integrative medicine research · 2023Review
- Fluorescent Sensing Platforms for Detecting and Imaging the Biomarkers of Alzheimer's Disease.Biosensors · 2023Review
- An aging, pathology burden, and glial senescence build-up hypothesis for late onset Alzheimer's disease.Nature communications · 2023Review
- Article
- Apoe4 and Alzheimer's Disease Pathogenesis-Mitochondrial Deregulation and Targeted Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Women and the risk of Alzheimer's disease.Frontiers in global women's health · 2023Review
- A multi-hit hypothesis for an APOE4-dependent pathophysiological state.The European journal of neuroscience · 2022Review
- Predicting conversion to Alzheimer's disease in individuals with Mild Cognitive Impairment using clinically transferable features.Scientific reports · 2022Article
- Analysis of differential gene expression and transcript usage in hippocampus of Apoe null mutant mice: Implications for Alzheimer's disease.Neuroscience research · 2022Article
- Apolipoprotein E4 Effects a Distinct Transcriptomic Profile and Dendritic Arbor Characteristics in Hippocampal Neurons CulturedFrontiers in aging neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The major genetic risk factor for sporadic Alzheimer's disease (AD) is the lipid binding and transporting carrier protein apolipoprotein E, epsilon 4 allele (ApoE4). One of the unsolved mysteries of AD is how the presence of ApoE4 elicits this age-associated, currently incurable neurodegenerative disease. Recently, we showed that ApoE4 acts as a transcription factor and binds to the promoters of genes involved in a range of processes linked to aging and AD disease pathogenesis. These findings point to novel therapeutic strategies for AD and aging, resulting in an extension of human healthspan, the disease-free and functional period of life. Here, we review the effects and implications of the putative transcriptional role of ApoE4 and propose a model of Alzheimer's disease that focuses on the transcriptional nature of ApoE4 and its downstream effects, with the aim that this knowledge will help to define the role ApoE4 plays as a risk factor for AD, aging, and other processes such as inflammation and cardiovascular disease.
Indexed as
Identifiers
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.