“…These include a significant dedication of medical personnel to individual AD patients in cooperation with family and caregivers, multiple combinatorial approaches including extensive clinical assessment, intermittent brain neuroimaging over the onset and course of AD and a host of multiple molecular, genetic, epigenetic, neurophysiological, and neurobiological strategies with focus on CSF, serum biomarkers, miRNA and perhaps other sncRNA abundance in these biofluid compartments. While significant progress is being made: it is important to point out that: (i) combinatorial diagnostic methodologies incorporating molecular genetic markers such as miRNA screening combined with DNA-based gene mutation analysis, advanced MRI-or PET-neuroimaging techniques and conscientious clinical evaluations, still have difficulty in the diagnosis of AD, often requiring the stratification of AD into complex subgroups and post-mortem verification (Guerreiro et al, 2012;Pogue and Lukiw, 2018;Penner et al, 2019;Peña-Bautista et al, 2019;Guest et al, 2020;Habes et al, 2020;Hampel et al, 2020a,b;Hudon et al, 2020;Khoury and Grossberg, 2020;Sherva et al, 2014;Rossini et al, 2020;Serpente et al, 2020;Sims et al, 2020;Singh and Yadav, 2020;Swarbrick et al, 2019;Turner et al, 2020;van den Berg et al, 2020;Weller, 2020); and (ii) currently available pharmacology and strategic treatments (including targeted drug delivery) based on these diagnostic tools, in the majority of cases, still do not directly address the primary underlying cause of either EOAD or LOAD but are sadly limited to the temporary alleviation of clinical symptoms (Di Resta and Ferrari, 2019;Veitch et al, 2019;Guest et al, 2020;Khoury and Grossberg, 2020;Lewczuk et al, 2020;Patnode et al, 2020;Rahman et al, 2020).…”