Indeed, increased levels of miR153-3p were found in the HP of a rat model of chronic brain hypoperfusion [38]—a condition often associated with age-related disease, such as Alzheimer’s disease (AD) and vascular dementia [39, 40]—and it has been demonstrated that this upregulation was causally related to decreased pre- and post-synaptic plasticity at the CA3-CA1 pathway, reduced expression of several vesicle fusion proteins and presynaptic proteins (SNAP-25, VAMP-2, syntaxin-1A and synaptotagmin-1, synapsin I) and altered synaptic vesicle trafficking [34, 38]. This evidence concerns the gene SNAP25 and early-onset autosomal dominant Alzheimer disease.