Biomedical research has sought to characterise and identify the biological basis of the pathophysiological process of AD and has, more recently, focused on how the peptide Aβ and the microtubule-associated protein tau form AD-characteristic senile plaques and neurofibrillary tangles and contribute to neuronal loss and neural degeneration (see, for example, Kametani and Hasegawa 2018). The gene discussed is MAPT; the disease is Alzheimer disease.