ArticleMolecular psychiatry2022
C/EBPβ/AEP signaling couples atherosclerosis to the pathogenesis of Alzheimer's disease.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.
- Meta-analysis and transcriptomic analysis reveal that NKRF and ZBTB17 regulate the NF-κB signaling pathway, contributing to the shared molecular mechanisms of Alzheimer's disease and atherosclerosis.CNS neuroscience & therapeutics · 2024Pooled it
- C/EBPβ: A transcription factor associated with the irreversible progression of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Pooled it
- The transcription factor C/EBPβ promotes hyperglycemia-elicited glycolysis and liver cancer progression.Nature communications · 2026Article
- Review
- Atractylenolide I mitigates Alzheimer's disease pathology in ApoEActa biochimica et biophysica Sinica · 2026Article
- C/EBPβ-VCAM1 axis in Kupffer cells promotes hepatic inflammation in MASLD.JHEP reports : innovation in hepatology · 2025Article
- APOE4 Exacerbates Cerebral Tau Pathology Through Cholesterol-Induced Degradation of Phosphatase in Atherosclerosis.CNS neuroscience & therapeutics · 2025Article
- Buyang Huanwu Decoction Modulates the Gut Microbiota-C/EBPβ/AEP Axis to Ameliorate Cognitive Impairment in Alzheimer's Disease Mice.CNS neuroscience & therapeutics · 2025Article
- Asparagine endopeptidase cleaves apolipoprotein A1 and accelerates pathogenesis of atherosclerosis.The Journal of clinical investigation · 2025Article
- Precision Prediction of Alzheimer's Disease: Integrating Mitochondrial Energy Metabolism and Immunological Insights.Journal of molecular neuroscience : MN · 2025Article
- Alisol A ameliorates vascular cognitive impairment via AMPK/NAMPT/SIRT1-mediated regulation of cholesterol and autophagy.Theranostics · 2025Article
- Roles of C/EBPβ/AEP in Neurodegenerative Diseases.Current topics in medicinal chemistry · 2025Review
- Article
- Atherosclerosis is associated with plasma Aβ levels in non-hypertension patients.BMC neurology · 2024Article
- Involvement of Fgf2-mediated tau protein phosphorylation in cognitive deficits induced by sevoflurane in aged rats.Molecular medicine (Cambridge, Mass.) · 2024Article
- Advances in pathogenesis and treatment of vascular endothelial injury-related diseases mediated by mitochondrial abnormality.Frontiers in pharmacology · 2024Review
- Association between atherosclerosis and the development of multi-organ pathologies.SAGE open medicine · 2024Review
- Sepsis exacerbates Alzheimer's disease pathophysiology, modulates the gut microbiome, increases neuroinflammation and amyloid burden.Molecular psychiatry · 2023Article
- Inflammation-activated C/EBPβ mediates high-fat diet-induced depression-like behaviors in mice.Frontiers in molecular 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
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Atherosclerosis (ATH) and Alzheimer's disease (AD) are both age-dependent inflammatory diseases, associated with infiltrated macrophages and vascular pathology and overlapping molecules. C/EBPβ, an Aβ or inflammatory cytokine-activated transcription factor, and AEP (asparagine endopeptidase) are intimately implicated in both ATH and AD; however, whether C/EBPβ/AEP signaling couples ATH to AD pathogenesis remains incompletely understood. Here we show that C/EBPβ/AEP pathway mediates ATH pathology and couples ATH to AD. Deletion of C/EBPβ or AEP from primary macrophages diminishes cholesterol load, and inactivation of this pathway reduces foam cell formation and lesions in aorta in ApoE-/- mice, fed with HFD (high-fat-diet). Knockout of ApoE from 3xTg AD mouse model augments serum LDL and increases lesion areas in the aorta. Depletion of C/EBPβ or AEP from 3xTg/ApoE-/- mice substantially attenuates these effects and elevates cerebral blood flow and vessel length, improving cognitive functions. Strikingly, knockdown of ApoE from the hippocampus of 3xTg mice decreases the cerebral blood flow and vessel length and aggravates AD pathologies, leading to cognitive deficits. Inactivation of C/EBPβ/AEP pathway alleviates these events and restores cognitive functions. Hence, our findings demonstrate that C/EBPβ/AEP signaling couples ATH to AD via mediating vascular pathology.
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.