Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung, 40402, Taiwan.
Department of Medical Research, China Medical University Hospital, Taichung, 40447, Taiwan.
Neurol Sci. 2019 Aug;40(8):1577-1582. doi: 10.1007/s10072-019-03879-3. Epub 2019 Apr 8.
Dementia is one of the diabetic complications under intensive study. Alteration of synaptic adhesion protein (SAP) associates with neurological diseases, including Alzheimer's disease. However, the regulation of SAPs in the brain of diabetes mellitus remains elusive. To pinpoint the candidate SAPs underlining the mechanism of diabetic dementia, we investigated expression profiling of SAPs in both streptozotocin (STZ)-induced diabetic mice, App mice, and amyloid precursor protein intracellular domain (AICD)-induced human neural cell line from public databases. DST (Dystonin/BPAG1) was identified upregulated in both models. Our finding suggests that DST alteration may involve in the mechanism of diabetic dementia.
痴呆是糖尿病并发症中研究较为集中的一种。突触黏附蛋白（SAP）的改变与包括阿尔茨海默病在内的神经疾病有关。然而，糖尿病患者大脑中 SAP 的调节仍不清楚。为了确定潜在的 SAPs 作为糖尿病性痴呆发病机制的线索，我们从公共数据库中研究了链脲佐菌素（STZ）诱导的糖尿病小鼠、APP 小鼠和淀粉样前体蛋白细胞内域（AICD）诱导的人神经细胞系中 SAP 的表达谱。发现 DST（dystonin/BPAG1）在这两种模型中均上调。我们的研究结果表明，DST 的改变可能与糖尿病性痴呆的发病机制有关。
