However, according to the cholinergic hypothesis in AD, excessive alterations inAChE alongside reduced cortical innervations, corticocortical glutamatergicneurotransmission, coupling of muscarinic M1 receptors to secondary messengersinside the post-synaptic neuron are contributory factors towards the aggravationof tau protein formation, amyloidogenesis, and amyloidosis which are symptomatichallmarks of AD [14]. The gene discussed is MAPT; the disease is Alzheimer disease.