BackgroundAlzheimer's disease (AD) is a neurodegenerative disorder distinguished by a swift cognitive deterioration accompanied by distinctive pathological hallmarks such as extracellular Aβ (β‐amyloid) peptides, neuronal neurofibrillary tangles (NFTs), sustained neuroinflammation, and synaptic degeneration. The elevated frequency of AD cases and its proclivity to manifest at a younger age present a pressing challenge in the quest for novel therapeutic interventions. Numerous investigations have substantiated the involvement of C/EBPβ in the progression of AD pathology, thus indicating its potential as a therapeutic target for AD treatment.AimsSeveral studies have demonstrated an elevation in the expression level of C/EBPβ among individuals afflicted with AD. Consequently, this review predominantly delves into the association between C/EBPβ expression and the pathological progression of Alzheimer's disease, elucidating its underlying molecular mechanism, and pointing out the possibility that C/EBPβ can be a new therapeutic target for AD.MethodsA systematic literature search was performed across multiple databases, including PubMed, Google Scholar, and so on, utilizing predetermined keywords and MeSH terms, without temporal constraints. The inclusion criteria encompassed diverse study designs, such as experimental, case–control, and cohort studies, restricted to publications in the English language, while conference abstracts and unpublished sources were excluded.ResultsOverexpression of C/EBPβ exacerbates the pathological features of AD, primarily by promoting neuroinflammation and mediating the transcriptional regulation of key molecular pathways, including δ‐secretase, apolipoprotein E4 (APOE4), acidic leucine‐rich nuclear phosphoprotein‐32A (ANP32A), transient receptor potential channel 1 (TRPC1), and Forkhead BoxO (FOXO).DiscussionThe correlation between overexpression of C/EBPβ and the pathological development of AD, along with its molecular mechanisms, is evident. Investigating the pathways through which C/EBPβ regulates the development of AD reveals numerous multiple vicious cycle pathways exacerbating the pathological progression of the disease. Furthermore, the exacerbation of pathological progression due to C/EBPβ overexpression and its molecular mechanism is not limited to AD but also extends to other neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and multiple sclerosis (MS).ConclusionThe overexpression of C/EBPβ accelerates the irreversible progression of AD pathophysiology. Additionally, C/EBPβ plays a crucial role in mediating multiple pathways linked to AD pathology, some of which engender vicious cycles, leading to the establishment of feedback mechanisms. To sum up, targeting C/EBPβ could hold promise as a therapeutic strategy not only for AD but also for other degenerative diseases.

中文翻译：

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C/EBPβ：与阿尔茨海默病不可逆进展相关的转录因子

背景阿尔茨海默病（AD）是一种神经退行性疾病，其特征是认知能力迅速恶化，并伴有独特的病理标志，例如细胞外 Aβ（β-淀粉样蛋白）肽、神经元神经原纤维缠结（NFT）、持续神经炎症和突触变性。 AD 病例发生频率的增加及其在年轻时发病的倾向，对寻求新的治疗干预措施提出了紧迫的挑战。大量研究证实了 C/EBPβ 参与 AD 病理进展，从而表明其作为 AD 治疗靶点的潜力。 目的 几项研究表明，AD 患者中 C/EBPβ 的表达水平升高。因此，本文主要探讨C/EBPβ表达与阿尔茨海默病病理进展之间的关系，阐明其潜在的分子机制，并指出C/EBPβ可能成为AD新的治疗靶点。方法系统文献检索是在多个数据库（包括 PubMed、Google Scholar 等）上进行的，利用预先确定的关键字和 MeSH 术语，没有时间限制。纳入标准涵盖多种研究设计，例如实验、病例对照和队列研究，仅限于英语出版物，而会议摘要和未发表的来源被排除在外。 结果 C/EBPβ 的过度表达会加剧 AD 的病理特征，主要是通过促进神经炎症和介导关键分子途径的转录调节，包括 δ-分泌酶、载脂蛋白 E4 (APOE4)、酸性富含亮氨酸的核磷蛋白 32A (ANP32A)、瞬时受体电位通道 1 (TRPC1) 和 Forkhead BoxO (FOXO) ).讨论 C/EBPβ 的过度表达与 AD 病理发展及其分子机制之间的相关性是显而易见的。研究 C/EBPβ 调节 AD 发展的途径揭示了许多多重恶性循环途径，加剧了该疾病的病理进展。此外，C/EBPβ过表达导致的病理进展加剧及其分子机制不仅限于AD，还延伸至其他神经退行性疾病，如肌萎缩侧索硬化症（ALS）、帕金森病（PD）和多发性硬化症（MS）结论 C/EBPβ的过度表达加速了AD病理生理学不可逆的进展。此外，C/EBPβ 在介导与 AD 病理相关的多种途径中发挥着至关重要的作用，其中一些途径会产生恶性循环，从而导致反馈机制的建立。总而言之，靶向 C/EBPβ 不仅有望成为 AD 的治疗策略，也有望成为其他退行性疾病的治疗策略。