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Several mutations in Cu, Zn-SOD gene are found to be associated with FALS.[66] In addition, Cu, Zn-SOD is one of the prime victims of oxidative damage to the brain in AD and Parkinsons disease.[67] It has been experimentally demonstrated that overexpression of SOD-2 reduces hippocampal superoxide and hence prevents memory deficits in a mouse model of AD.[68] SOD supplementation showed improvement in mice model of AD.[69] SOD/catalase mimetic EUK-207 exhibited protection against and interruption of progression of amyloid and tau pathology and cognitive decline in a mouse model of AD.[70] SOD and diabetes Increased oxidative stress plays a major role in the etiology of diabetes and its complications.[71-73] In diabetes, persistent hyperglycemia stimulates the production of ROS from various sources.[74] As a result, diabetes usually leads to increased formation of ROS and weakened antioxidant defenses.[75,76] SOD catalyzes the conversion of O 2 - into H 2 O 2

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Additionally, BPC 157 may participate in the braingut and gutbrain axis function [9], exerting particular effects when given peripherally [9] (i.e., release of the serotonin in the specific brain areas (i.e., nigrostriatum) [31], opposes the schizophrenia-like positive symptoms models [32], counteracts various encephalopathies [30,33,34,35,36,37,38,39,40,41])