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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\/EBP\u03b2 in the progression of AD pathology, thus indicating its potential as a therapeutic target for AD treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aims<\/jats:title><jats:p>Several studies have demonstrated an elevation in the expression level of C\/EBP\u03b2 among individuals afflicted with AD. Consequently, this review predominantly delves into the association between C\/EBP\u03b2 expression and the pathological progression of Alzheimer's disease, elucidating its underlying molecular mechanism, and pointing out the possibility that C\/EBP\u03b2 can be a new therapeutic target for AD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>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\u2013control, and cohort studies, restricted to publications in the English language, while conference abstracts and unpublished sources were excluded.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Overexpression of C\/EBP\u03b2 exacerbates the pathological features of AD, primarily by promoting neuroinflammation and mediating the transcriptional regulation of key molecular pathways, including \u03b4\u2010secretase, apolipoprotein E4 (APOE4), acidic leucine\u2010rich nuclear phosphoprotein\u201032A (ANP32A), transient receptor potential channel 1 (TRPC1), and Forkhead BoxO (FOXO).<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>The correlation between overexpression of C\/EBP\u03b2 and the pathological development of AD, along with its molecular mechanisms, is evident. Investigating the pathways through which C\/EBP\u03b2 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\/EBP\u03b2 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).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The overexpression of C\/EBP\u03b2 accelerates the irreversible progression of AD pathophysiology. Additionally, C\/EBP\u03b2 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\/EBP\u03b2 could hold promise as a therapeutic strategy not only for AD but also for other degenerative diseases.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.14721","type":"journal-article","created":{"date-parts":[[2024,4,22]],"date-time":"2024-04-22T04:49:37Z","timestamp":1713761377000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["C\/<scp>EBP\u03b2<\/scp>: A transcription factor associated with the irreversible progression of Alzheimer's disease"],"prefix":"10.1111","volume":"30","author":[{"given":"Qing","family":"Yao","sequence":"first","affiliation":[{"name":"Department of Anesthesiology The Second Affiliated Hospital of Nanchang University  Nanchang City Jiangxi Province China"},{"name":"Key Laboratory of Anesthesiology of Jiangxi Province  Nanchang City Jiangxi Province 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