In this context, administering OTA activates various pathways including p38 mitogen-activated protein kinases (MAPK) and Jun N-terminal Kinases (JNK), causes Extracellular-Signal-Regulated Kinase (ERK) dysfunction, disrupts brain-derived neurotrophic factor (BDNF), is related to Tyrosine hydroxylase (TH) overexpression, and caspase-3 and 9 activation, as well as ERK-1/2 phosphorylation which ultimately leads to the progression of Alzheimer’s disease (AD) [76]. The gene discussed is BDNF; the disease is early-onset autosomal dominant Alzheimer disease.