2016-06-012024-05-18https://scholars.lib.ntu.edu.tw/handle/123456789/703010摘要：N-methyl-D-aspartic Acid (NMDA) 受體調節功能低下已經被報告為精神分裂症疾病的神經病理症狀之一，此受體為離子通道由兩種蛋白質以四個聚合體組成NMDA受體1 (NR1)以及受體2 (NR2)，NR1受體與共同促效劑 (co-agonist) glycine結合，而NR2受體則結合穀氨酸鹽 (glutamate)共同調節NMDA受體離子通道的開關，調節NR1受體的glycine結合位址，可以改善精神分裂症病人的認知功能以及負性症狀。D-胺基酸氧化&#37238;代謝NR1受體的glycine結合位址的D-serine 共同促效劑，抑制D-胺基酸氧化&#37238;可以提高D-serine在神經突觸間隙的濃度，進而提高NMDA受體的功能，改善負性症狀以及認知功能。<br> Abstract: The reduction regulatory mechanism of glutamate transmission on N-methyl-D-aspartic Acid (NMDA) receptor has been reported as one of the neuropathology in schizophrenia. The receptor is an ion channel with heterotetramer of two structure subunits of NMDA receptor 1 (NR1) and NR2. The NR1 binds the co-agonist glycine and the NR2 binds the neurotransmitter glutamate to regulate the ion channel opening. Modulation the glycine binding site of NR1 may improve cognitive function and negative symptoms in schizophrenia. D-amino acid oxidase (DAO) metabolizes D-serine of a co-agonist at the glycine NR1 binding site. Inhibiting DAO may increase D-serine in the synaptic cleft, enhance the NMDA receptor activity and improve negative and cognitive symptoms. Antipsychotic combining D-serine has been reported effective in treatment of schizophrenia.N-methyl-D-aspartic Acid (NMDA) 受體D-胺基酸氧化&#37238D-胺基酸氧化&#37238抑制劑臨床前試驗RS-D7N-methyl-D-aspartic Acid (NMDA) receptorD-amino acid oxidase (DAO)DAO inhibitor (DAOI)preclinical trialRS-D7