Sera miR-34a, miR-29b and miR-181c as potential novel diagnostic biomarker panel for Alzheimers in the Egyptian population

生物标志物 诊断准确性 医学 内科学 诊断生物标志物 肿瘤科 小RNA 阿尔茨海默病 疾病 人口 生物 遗传学 环境卫生 基因
作者
Nermeen Z. Abuelezz,Fayza Eid Nasr,Waleed M. Abdel Aal,Tarek Molokhia,Amira Zaky
出处
期刊:Experimental Gerontology [Elsevier]
卷期号:169: 111961-111961 被引量:15
标识
DOI:10.1016/j.exger.2022.111961
摘要

Till date, there is an obvious obscurity of specific and early diagnostic biomarkers for Alzheimer's disease (AD). The promising diagnostic potential of serum miRNAs is increasingly emerging; however, rare miRNAs data originates from middle and low-income countries to provide proper validation in these highly affected populations. This study evaluated the diagnostic value of serum miR-34a, miR-29b and miR-181c in Egyptian AD patients.Expression levels of serum miR-34a, miR-29b and miR-181c were determined using quantitative real time PCR in AD patients versus healthy controls. Amyloid Beta 42 (Aβ42), Phosphorylated Tau (p-Tau) and TNF-α levels were also detected as distinctive AD markers. We further explored the correlation between miRNAs levels and Mini mental state examination (MMSE) scores. Finally, we conducted logistic regression and ROC curve analyses to evaluate the diagnostic values of the measured parameters.Sera miR-34a, miR-29b and miR-181c were significantly downregulated in AD patients and this decrease was associated with cognitive decline. AD patients manifested significant elevation of Aβ42, pTau and TNF-α levels. The measured miRNAs showed good AD diagnostic value solely and when used together (AUC = 0.77, 95 % C·I. 0.62-0.93 at p < 0.01). Interestingly, combining miRNAs panel with Aβ42, TNF-α and pTau levels remarkably increased the diagnostic power (AUC = 0.97, 95 % C·I. 0.94-1.00 at p < 0.001) achieving sensitivity 88.2 % and specificity 91.4 %.This study spots for the first time the diagnostic potential of serum miR-34a, miR-29b and miR-181c as minimally invasive AD biomarker panel in Egyptian patients and highlights their contribution in AD pathogenesis.

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