[Neurogenic mechanisms of development of type 1 diabetes mellitus]

Immunohistochemical (tests for insulin, glucagons, periferin, SNAP-25, GFAP, NGF-R, RMR-22, MBP) and morphological studies were performed to examine the pancreatic nervous apparatus of human adults and fetuses in late phases of development. A role of the morphogenetic activity of the pancreatic nervous apparatus was investigated in type 1 diabetes mellitus (DM-1). The neurons and gliocytes located in the pancreas are suggested to have a morphogenetic activity and form a glial capsule throughout their life. The insular endocrine cells are shown to synthesize the proteins (SNAP-25, GFAP) characteristic of nerve cells and their synaptic terminals. A neurobiological model of DM-1 'development has been stated. The onset of the disease is characterized by the development of autoimmune processes directed to the nervous system. In nerve tissue protein autoimmunization, the fine insular neuroglial membrane is rapidly disrupted. This leads to the transfer of autoimmune aggression to the insulin-producing cells of the islets of Langerhans, which carry specific nerve tissue proteins onto their surface. Recovery of the islets becomes impossible without forming a protective neuroglial membrane, which makes the development of DM-1 irreversible.