The pathophysiology of Alzheimer’s disease (AD) is characterized by a formation of extracellular amyloid plaques in the cortex and limbic system, aggregation of hyperphosphorylated τ-protein causing intracellular neurofibrillary tangles and is often accompanied by reactive microgliosis and loss of synapses, cholinergic, serotonergic, and noradrenergic function together with glutamatergic dysfunction (López and DeKosky, 2008; Reitz and Mayeux, 2014; Vaňková et al., 2016). Here, TBXT is linked to Alzheimer disease.