Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. ====== MEF2C ====== [[Myocyte]] enhancer factor 2C (MEF2C) is highly expressed in the [[nervous system]], and regulates neuro-development, [[synaptic plasticity]], and [[inflammation]]. However, its mechanism in [[Alzheimer's disease]] (AD) is underestimated. In a study, the role and mechanism of MEF2C were investigated in the [[brain tissue]] specimens from patients with AD, [[APPswe]]/[[PSEN1dE9]] double transgenic (APP/PS1_DT) mice, and [[SH-SY5Y]] cells treated with [[amyloid beta]] [[peptide]] (Aβ). The results indicated that the expression of MEF2C is significantly reduced, and the expression of MEF2C/Aβ in different parts of brain is negatively correlated in patients with AD. [[Knockdown]] of MEF2C promotes [[cell]] [[apoptosis]] and the level of β-amyloid precursor protein cleaving enzyme 1 ([[BACE]]) but reduces BACE2 expression. In addition, knockdown of enhances the generation and aggregation of Aβ in the cortex of APP/PS1_DT [[mice]], reduces the expression of synaptic proteins, exacerbates the ability of learning and memory of APP/PS1_DT mice, damages the structure of [[mitochondria]], increases the [[oxidative stress]] (OS) level, and inhibits the expression levels of members of the [[Nrf2]]-ARE signal pathway. In summary, inhibition of MEF2C exacerbates the toxic effect of Aβ and , damages [[synaptic plasticity]], reduces the ability of learning and memory of APP/PS1 mice, and increases the level of OS via the Nrf2-ARE signal pathway ((Ren J, Zhang S, Wang X, Deng Y, Zhao Y, Xiao Y, Liu J, Chu L, Qi X. MEF2C ameliorates learning, memory, and molecular pathological changes in Alzheimer's disease and. Acta Biochim Biophys Sin (Shanghai). 2022 Jan 25;54(1):1-14. doi: 10.3724/abbs.2021012. PMID: 35130621.)). mef2c.txt Last modified: 2024/06/07 02:55by 127.0.0.1