GAD1 and type 1 diabetes mellitus: Furthermore, autoimmune mechanisms are hypothesized to contribute to neural damage in T1DM, as the presence of autoantibodies against glutamic acid decarboxylase (GAD) and islet antigen-2 (IA-2) could represent a distinct pathophysiological mechanism for axonal degeneration development in T1DM-associated DSPN [42].