Low levels of BDNF have been related to many diseases such as AD because such levels induce a decrease in mitochondrial biogenesis, neuronal survival, and plasticity associated with a deficiency in the TrkB signaling receptor by different pathways: MAPK, a regulator of neuronal differentiation and maturation; PI3K, important in neuronal survival and synaptic protein formation; and PLCγ, which induces the release of intracellular Ca2+ related to synaptic plasticity [108]. This evidence concerns the gene BDNF and Alzheimer disease.