PDF(Pubmed)
Abstract：
Alzheimer\'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.
Several 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.
A 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case-control, and cohort studies, restricted to publications in the English language, while conference abstracts and unpublished sources were excluded.
Overexpression 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).
The 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).
The 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.
Several 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.
A 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.
Overexpression 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).
The 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).
The 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.
摘要：
背景：阿尔茨海默病（AD）是一种神经退行性疾病，其特征是迅速的认知退化，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），持续的神经炎症，和突触变性.AD病例的频率升高及其在年轻时表现出的倾向在寻求新的治疗干预措施方面提出了紧迫的挑战。大量研究证实了C/EBPβ参与AD病理的进展。因此表明其作为AD治疗的治疗靶标的潜力。
目的：一些研究表明，患有AD的个体中C/EBPβ的表达水平升高。因此,这篇综述主要探讨了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：在多个数据库中进行了系统的文献检索，包括PubMed,谷歌学者，等等，利用预定的关键词和MeSH术语，没有时间限制。纳入标准包括不同的研究设计，比如实验性的，病例控制，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过表达加重了AD的病理特征，主要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），和叉头盒(FOXO)。
结论：C/EBPβ过表达与AD病理发展的相关性。连同其分子机制，很明显。研究C/EBPβ调节AD发展的途径揭示了许多多个恶性循环途径，加剧了疾病的病理进展。此外，C/EBPβ过表达引起的病理进展恶化及其分子机制不仅限于AD，还扩展到其他神经退行性疾病，例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的过表达加速了AD病理生理学的不可逆进展。此外,C/EBPβ在介导与AD病理相关的多个途径中起着至关重要的作用，其中一些会产生恶性循环，导致反馈机制的建立。总而言之,靶向C/EBPβ不仅有望作为AD的治疗策略，也有望作为其他退行性疾病的治疗策略。
目的：一些研究表明，患有AD的个体中C/EBPβ的表达水平升高。因此,这篇综述主要探讨了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：在多个数据库中进行了系统的文献检索，包括PubMed,谷歌学者，等等，利用预定的关键词和MeSH术语，没有时间限制。纳入标准包括不同的研究设计，比如实验性的，病例控制，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过表达加重了AD的病理特征，主要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），和叉头盒(FOXO)。
结论：C/EBPβ过表达与AD病理发展的相关性。连同其分子机制，很明显。研究C/EBPβ调节AD发展的途径揭示了许多多个恶性循环途径，加剧了疾病的病理进展。此外，C/EBPβ过表达引起的病理进展恶化及其分子机制不仅限于AD，还扩展到其他神经退行性疾病，例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的过表达加速了AD病理生理学的不可逆进展。此外,C/EBPβ在介导与AD病理相关的多个途径中起着至关重要的作用，其中一些会产生恶性循环，导致反馈机制的建立。总而言之,靶向C/EBPβ不仅有望作为AD的治疗策略，也有望作为其他退行性疾病的治疗策略。
