Ask about this productRelated genes to: ApoE antibody
- Gene:
- APOE NIH gene
- Name:
- apolipoprotein E
- Previous symbol:
- AD2
- Synonyms:
- -
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: ApoE antibody
Related articles to: ApoE antibody
- Atherosclerotic cardiovascular disease is still a major cause for the increasing mortality worldwide. The elevated metabolite N-acetylneuraminic acid (Neu5Ac) was considered one of the important risk factors responsible for the initiation of endothelial impairment, then participated in atherosclerosis progression. However, the reason for inducing Neu5Ac accumulation as well as its underlying mechanism remains unclear. Here, we applied human umbilical vein endothelial cells (HUVECs) and ApoE mice to investigate the key genes responsible for Neu5Ac accumulation as well as its regulation mechanism. We found that tumour necrosis factor alpha (TNF-α) could induce Neu5Ac metabolism disorder and increase Neu5Ac level, accompanied by the increasing levels of inflammatory markers in HUVECs. Further, we found that sialidase NEU3 was significantly up-regulated, accompanied by Neu5Ac accumulation. NEU3 in HUVECs could significantly reduce Neu5Ac levels and alleviate endothelial inflammation. In contrast, the addition of exogenous Neu5Ac reversed such phenomenon. Furthermore, we noted that NEU3 was highly expressed in atherosclerotic plaques from ApoE mice as well as atherosclerotic patient tissues. Mechanically, we found that the transcription factor specificity protein 3 (SP3) was activated in HUVECs, responsible for Neu5Ac metabolism disorder. While RNA interference of SP3 could decrease NEU3 mRNA level and reduce endothelial inflammatory injury, indicating that SP3 might be the upstream regulatory factor of NEU3. Together, these findings identified the key role of NEU3 in regulating Neu5Ac metabolism associated with endothelial function, as well as its potential regulation mechanism. Targeting SP3/NEU3 seems to be a potential therapeutic strategy for such diseases with Neu5Ac accumulation like atherosclerosis (AS). - Source: PubMed
Lu YiningXiang PengChen QingqiuWang XianminChen LeWang TongchuanHu RongMa LimeiYu Chao - Our study aimed to systematically identify T1-weighted MRI-derived brain structural features associated with progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD). - Source: PubMed
Publication date: 2026/05/11
Wang YanxiaSong WangchenYang XinyuMeng WeijingMa YonghuaWang AiminGuo GuiyaZhang ZhaoxueLi ZihuiHan HairuiWang SuzhenShi Fuyan - The etiology of Alzheimer's disease (AD) remains a subject of intense investigation. While the 2024 Lancet Commission report attributes approximately 45% of global dementia cases to 14 modifiable risk factors, it notably excludes infectious agents due to debated causality. This exclusion contrasts with growing evidence that pathogens, specifically Herpes Simplex Virus Type 1 (HSV-1), Porphyromonas gingivalis, and Chlamydia pneumoniae, may contribute to neuroinflammation, tau pathology and amyloidogenesis. This paper evaluates the Pathogen Hypothesis of AD through a quantitative framework. Synthesizing data from nationwide cohort studies, we apply a Population Attributable Fraction (PAF) model to estimate the potential disease burden associated with infectious agents. Our sensitivity analyses, utilizing E-values to quantify robustness against unmeasured confounding, suggest that, under the assumption of causality, infectious agents yield illustrative PAF scenarios ranging from 19% to 31% from single-pathogen models, which expands to 31% to 52% in joint models of sporadic AD cases. We explicitly model the heterogeneity between cohorts and the synergistic interaction with the APOE ε4 allele. Furthermore, we address recent failures in antimicrobial clinical trials (VALAD, GAIN), arguing that these outcomes reflect a need for precision biomarker stratification rather than a refutation of the hypothesis. These findings argue for the integration of precision pathogen suppression into dementia prevention protocols. - Source: PubMed
Publication date: 2026/05/11
Bender OmerShemesh Or ABar Daniel Z - Huangqi Chifeng Tang (HQCFT) has been demonstrated to exert anti-atherosclerotic (AS) effects through its lipid-lowering and anti-inflammatory activities. A multi-source data weighted target screening model was established based on chemical composition analysis to determine the priority of HQCFT active components and their targets. The anti-AS efficacy of HQCFT in ApoE mice was assessed by measuring blood lipids and evaluating aortic and liver histopathology. Aortic proteomics analysis was performed, and the results were intersected with weighted model predictions. Key targets were validated by RT-qPCR, Western blot, and molecular docking. The weighted model pinpointed high-contribution targets such as LGALS3, TNF, and HMGCR, along with key components including calycosin-7-O-β-D-glucoside and quercetin. HQCFT ameliorated dyslipidemia, aortic plaque formation, and hepatic steatosis in vivo. Mechanistically, HQCFT reduces serum inflammatory factor levels and inhibits LGALS3 mediated NLRP3 inflammasome pathway activation. Furthermore, HQCFT modulated lipid metabolism by inhibiting cholesterol and fatty acid synthesis via the HMGCR/ACC1 pathways, while promoting fatty acid β-oxidation through PPARα/CPT1A activation. These in vivo findings were further validated by in vitro experiments. In ox-LDL-induced VSMC foam cells, HQCFT reduced lipid accumulation and inhibited the LGALS3/NLRP3 mediated inflammatory response. In LPS-stimulated RAW264.7 macrophages, HQCFT suppressed M1 polarization and inhibited inflammatory activation. In FFA-induced HepG2 cells, HQCFT treatment reduced lipid accumulation, downregulated the expression of HMGCR, ACC1, and CD36, and upregulated the expression of LDLR, PPARα, and CPT1A. Finally, molecular docking confirmed strong binding interactions between HQCFT components and these key targets. Collectively, HQCFT exerts anti-atherosclerotic effects through a multi-component, multi-target mechanism involving inhibition of LGALS3 mediated NLRP3 inflammasome activation, suppression of VSMC foam cell formation, and coordinated regulation of hepatic lipid metabolism. The weighted screening model used here offers a quantitative approach for evaluating component contributions and target prioritization in traditional Chinese medicine research. - Source: PubMed
Publication date: 2026/05/11
Liang YuqinJiang XinLiu JieLu FangChen PingpingLiu Shumin - Human milk is a bioactive fluid containing maternal leukocytes that support infant immune protection and development. Prior work has demonstrated the presence of atypical, non-granulocyte milk myeloid cells that do not conform to previously-defined cell subsets. To assess the true diversity of mononuclear milk myeloid cells, we performed single-cell RNA sequencing (scRNAseq) on >23,000 CD45 ⁺ enriched cells from 9 healthy lactating donors. Clustering identified 18 transcriptionally distinct mononuclear myeloid subpopulations, including 10 macrophage clusters, 5 dendritic cell subsets, 1 monocyte population, and 2 epithelial-like clusters. Macrophages segregated into M1-like and M2-like states exhibiting discrete transcriptional programs. The epithelial-like clusters expressed both epithelial markers (e.g., EPCAM, KRT19, CLDN3) and myeloid genes, suggesting phagocytic activity or hybrid states. Numerous myeloid sub-clusters exhibited transcriptional features consistent with adaptation to the lipid-rich environment of milk, supported also by reactome data. This included LDL and lipoprotein clearance pathways and expression of genes such as INSIG1 and QSOX1 in monocytes and APOE, LIPA, and APOC1 in macrophages. Signaling pathways were also dominated by degranulation and IL-4/10/13 activities, as well as antigen presentation programs. CellChat analysis revealed extensive intercellular communication among myeloid subsets involving MHC-II, SPP1, and MIF, consistent with active antigen presentation and tissue remodeling. Notably, pronounced donor-specific heterogeneity was observed, with several sub-clusters restricted to 1-2 individuals, underscoring personalized immune composition during lactation. These data indicate that milk myeloid cells are not merely passively transported immune cells but actively shaped and diversified by the lactational niche, and establish a high-resolution framework for future studies. - Source: PubMed
Publication date: 2026/05/11
Schrode NadineYang XiaoqiFox AlisaChowhan DishaDeCarlo ClaireBeaumont KristinPowell Rebecca L R