Objectives: Diabetes mellitus has been associated with increased risk of cognitive decline, dementia, depression and anxiety. The aims of this study were to determine the influence of aging and long-term type 1 diabetes mellitus (DM1) on the rate of adult neurogenesis in subventricular zone of rats, as well as to determine the possible role of DSTYK protein in the adult neurogenesis in subventricular zone of rats as a possible disease mechanism. Material and Methods: Thirty-five male Sprague-Dawley rats randomly divided into two groups: control or diabetic. DM1 was induced by intraperitoneal injection of streptozotocin (55 mg/kg). DM1 was confirmed by measuring of plasma glucose 4 days after induction. Rats were sacrificed 2 weeks, 6 months and 1 year after induction of the DM1. Tissues of brain were processed for the immunohistochemistry for doublecortin (DCX) alone, or in combination with DSTYK. Results: For the thick part of the subependymal layer of the SVZ, the percentage of DCX area in the sections from a control group significantly decreased 6 months in comparison to the 2 weeks after the beginning of the experiment (P<0.01). For the thin part of the SVZ we measured the ratios of DCX staining surface to total nuclear surface. At two weeks and at 6 months the differences between the controls and the diabetic rats were not statistically significant. At 1 year there was a significant decrease (P = 0.025) between the controls and diseased animals. We also observed significant increase (P=0.045) comparing neurogenesis at 6 months and 1 year within the within the control group. DSTYK immunoreactivity was restricted to a wall of the brain blood vessels, the cells of the pia mater, as well as in glia of the white matter in different parts of the brain and spinal cord. In addition, we found expression of DSTYK on a regular base in ependymal cells of the central canal of the spinal cord and lateral ventricles of the brain. We did not find any signs of co-localization of the DSTYK with DCX, a marker for the neuroblasts in any of studied groups of animals. Conclusion: We concluded that long term experimental DM1 is decreasing neurogenesis in thin part of the SVZ in rat brain, while the short term DM1 did not have influence. Hence, short term studies are not relevant in conclusions for the influence of DM1 on neurogenesis in SVZ of rat. Ageing has an influence on neurogenesis in thick part of the SVZ of the rat brain and pattern of changes is bi-phasic, with initial transient decrease and increase in age of 14 months. DSTYK is expressed in rat brain in neurogenic areas of the SVZ, hence could have role in initial steps of the adult neurogenesis. Since DSTYK is not expressed in neuroblasts, it probably does not have role in their differentiation.