Through in silico analysis, we predicted that selected lncRNAs (Table 4) interact with possible target genes and impact their participation in different pathways that integrate the pathogenic network of AD (i.e., neurogenesis, cell differentiation, proteostasis of Aβ peptide and p-Tau, neuroinflammation, chromatin remodeling, neurite outgrowth, synaptic plasticity, apoptosis, and cell cycle control) and situations favoring AD development (i.e., depression, ciliopathies, and alteration of the intestinal barrier) (Table 5). This evidence concerns the gene MAPT and Alzheimer disease.