Studies of synapses in Alzheimer’s disease (AD) [61–64], dementia with Lewy bodies [65], and amyotrophic lateral sclerosis [66] demonstrated changes in synaptic density and morphology as well as molecular composition and the aggregation of disease-associated proteins in the synapse which may disrupt its structure and function. The gene discussed is PROS1; the disease is amyotrophic lateral sclerosis.