AUTOIMMUNE MECHANISMS IN DIABETIC NEUROPATHY

点击翻译按钮获取中文摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Diabetes mellitus is a very common disease caused by a lack of the hormone insulin (which regulates sugar) or an inability of tissues to use insulin. Five to 15 years after being diagnosed with diabetes most patients develop some type of complications involving the eyes, kidneys, nervous system and/or skin. These complications can be debilitating and costly. Nerve damage is one of the most common complications of diabetes and can affect the nerves of the hands and feet, as well as the nerves that regulate internal organs and vital body functions. In our laboratory, recent studies indicate that, in diabetics, there is increased calcium inside nerve cells (neurons) and increased nerve cell death. We have reason to believe that the body's own immune system may contribute to these problems. Therefore we wish to analyze the blood from insulin dependent and non-insulin dependent diabetic patients with and without nerve damage and compare it to the blood from normal healthy blood donors. We will be looking for proteins (antibodies) found in the blood, produced by the immune system. Through this study we hope to gain a better understanding of factors in the blood that may lead to nerve damage in diabetes mellitus and that may eventually aid in new treatments.