{Reference Type}: Journal Article
{Title}: Sera miR-34a, miR-29b and miR-181c as potential novel diagnostic biomarker panel for Alzheimers in the Egyptian population.
{Author}: Abuelezz NZ;Nasr FE;Abdel Aal WM;Molokhia T;Zaky A;
{Journal}: Exp Gerontol
{Volume}: 169
{Issue}: 0
{Year}: 11 2022
{Factor}: 4.253
{DOI}: 10.1016/j.exger.2022.111961
{Abstract}: 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.