Ranjbar Samira, Mohammadi Pantea, Pashaei Somayeh, Sadeghi Masoud, Mehrabi Masomeh, Shabani Sasan, Ebrahimi Ali, Brühl Annette B, Khodarahmi Reza, Brand Serge
Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah 6714415185, Iran.
Department of Clinical Biochemistry, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah 6714415185, Iran.
Biology (Basel). 2025 Apr 17;14(4):436. doi: 10.3390/biology14040436.
Exposure to aflatoxin (AF) triggers the production of inflammatory molecules and free radicals, leading to chronic inflammation, cancer, and neurodegenerative diseases. This systematic review evaluated the effects of AFB1 on the nervous system, particularly focusing on Alzheimer's disease (AD). A comprehensive search was conducted in Scopus, Cochrane Library, PubMed, and Web of Science databases up to 1 June 2024, without restrictions. From 993 records retrieved, 16 articles were included in the systematic review. AFB1 participates in various biochemical processes and pathological conditions. The study highlights that AFB1 contributes to AD by inducing DNA damage, oxidative stress, and endoplasmic reticulum (ER) stress, impairing DNA repair mechanisms. This results in neuronal damage, cognitive decline, and neurodegeneration. AFB1 also affects key signaling pathways, reduces sodium-potassium pump activity, and disrupts cell cycle regulation involving p53, leading to neurotoxicity, inflammation, and the formation of amyloid-beta (Aβ) plaques and neurofibrillary tangles. Additionally, network analysis revealed 309 genes associated with AD, inflammation, angiopathy, and aflatoxin B1 (AFB1). Among these, ESR1 exhibited the highest number of direct connections to other nodes within the network. The gene TP53 played a pivotal role in mediating communication among genes, while the EP300 gene significantly influenced the overall network structure. Additionally, KEGG enrichment analysis demonstrated that these 309 genes are substantially involved in pathways related to cancer, the FoxO signaling pathway, apoptosis, and AD. In summary, the study highlights that AFB1 causes DNA damage and stress, leading to cognitive decline and neurodegeneration. It disrupts signaling pathways, damages neurons, and affects DNA repair, contributing to neurotoxicity and inflammation. PROSPERO registration number: CRD420250651007.
接触黄曲霉毒素（AF）会引发炎症分子和自由基的产生，导致慢性炎症、癌症和神经退行性疾病。本系统评价评估了黄曲霉毒素B1（AFB1）对神经系统的影响，尤其关注阿尔茨海默病（AD）。截至2024年6月1日，在Scopus、Cochrane图书馆、PubMed和Web of Science数据库中进行了全面检索，无任何限制。在检索到的993条记录中，有16篇文章被纳入该系统评价。AFB1参与各种生化过程和病理状况。该研究强调，AFB1通过诱导DNA损伤、氧化应激和内质网（ER）应激，损害DNA修复机制，从而导致AD。这会导致神经元损伤、认知能力下降和神经退行性变。AFB1还会影响关键信号通路，降低钠钾泵活性，并破坏涉及p53的细胞周期调控，导致神经毒性、炎症以及淀粉样β（Aβ）斑块和神经原纤维缠结的形成。此外，网络分析揭示了309个与AD、炎症、血管病和黄曲霉毒素B1（AFB1）相关的基因。其中，ESR1与网络内其他节点的直接连接数量最多。基因TP53在介导基因间通信中起关键作用，而EP300基因对整体网络结构有显著影响。此外，KEGG富集分析表明，这309个基因大量参与与癌症、FoxO信号通路、细胞凋亡和AD相关的途径。总之，该研究强调AFB1会导致DNA损伤和应激，从而导致认知能力下降和神经退行性变。它会破坏信号通路，损害神经元，并影响DNA修复，进而导致神经毒性和炎症。PROSPERO注册号：CRD420250651007。
