HomeAbout us Research&Development Sarcopenia Scientific Background Investors Careers News Contact The treatment of age-related muscle atrophy (Sarcopenia) is a growing market with no available causal treatment. Sarcopenia and related disorders represent a current patient population of more than 10 million people. With age, progressive muscle deterioration leads to reduced muscular strength and is a major contributor to disability and frailty in the elderly, resulting eventually in loss of independence with associated increased health costs. Sarcopenia also plays an important role in the pathogenesis of decreased metabolic rate, gradual reduction of bone density and decreased aerobic capacity that occurs with old age. Recent research indicates that a dysfunction of the neuromuscular junction may be a major element in the pathogenesis of Sarcopenia. Correcting Sarcopenia by Tuning of Neurotrypsin Activity Research at Neurotune indicates, that sarcopenia may be caused by excessive activity of Neurotrypsin. Neurotrypsin is a synaptic serine protease that has a synapse-destabilizing function. Thus, Neurotrypsin is an essential regulatory element in the subtle, tightly controlled interplay between pro- and anti-synaptic forces resulting in synaptic homeostasis. A synaptic disorder is the consequence of dysregulation exceeding a threshold. A regulatory dysbalance with excessive synapse-destabilizing activity at the neuromuscular junction results in deterioration of the neuromuscular junction and subsequently in Sarcopenia-type skeletal muscle atrophy. Therefore, the pharmacological tuning of neurotrypsin is expected to have a beneficial effect on age-dependent muscle fiber denervation, muscle fiber loss, and skeletal muscle atrophy. © Copyright by Neurotune Switzerland