日本愛知縣身心障礙者精神發(fā)育障礙研究所日前宣布,，該所研究人員發(fā)現(xiàn)了與精神分裂癥發(fā)病有關(guān)的一種蛋白質(zhì)的功能,從而弄清了此病的發(fā)病機(jī)制,。
精神分裂癥是以幻覺和妄想為癥狀的精神疾病,。雖然神經(jīng)傳導(dǎo)物質(zhì)分泌異常和腦神經(jīng)發(fā)育障礙被認(rèn)為是致病原因，但是研究人員過去一直沒有弄清詳細(xì)的發(fā)病機(jī)制,。
在本次研究中，研究人員發(fā)現(xiàn)，蛋白質(zhì)“Dysbindin－1”與精神分裂癥發(fā)病有關(guān),，這種蛋白質(zhì)存在于負(fù)責(zé)腦神經(jīng)細(xì)胞間信息交換的“突觸”中。
研究人員通過老鼠實(shí)驗(yàn)發(fā)現(xiàn),，減少“Dysbindin－1”蛋白質(zhì)的含量,，在“突觸”中接受信息的組織就無(wú)法正常發(fā)育，從而導(dǎo)致精神分裂癥,。反之,，如果補(bǔ)充這種蛋白質(zhì)，有關(guān)組織的機(jī)能就會(huì)得到恢復(fù),。
有關(guān)論文已刊登在英國(guó)《分子精神病學(xué)》網(wǎng)絡(luò)版上,。(生物谷Bioon.net)
生物谷推薦原文出處：
Molecular Psychiatry doi: 10.1038/mp.2010.69
Dysbindin-1, WAVE2 and Abi-1 form a complex that regulates dendritic spine formation
H Ito1, R Morishita1, T Shinoda1, I Iwamoto1, K Sudo1, K-I Okamoto1 and K Nagata1
1Department of Molecular Neurobiology, Institute for Developmental Research, Aichi Human Service Center, Kasugai, Aichi, Japan
Genetic variations in dysbindin-1 (dystrobrevin-binding protein-1) are one of the most commonly reported variations associated with schizophrenia. As schizophrenia could be regarded as a neurodevelopmental disorder resulting from abnormalities of synaptic connectivity, we attempted to clarify the function of dysbindin-1 in neuronal development. We examined the developmental change of dysbindin-1 in rat brain by western blotting and found that a 50?kDa isoform is highly expressed during the embryonic stage, whereas a 40?kDa one is detected at postnatal day 11 and increased thereafter. Immunofluorescent analyses revealed that dysbindin-1 is enriched at the spine-like structure of primary cultured rat hippocampal neurons. We identified WAVE2, but not N-WASP, as a binding partner for dysbindin-1. We also found that Abi-1, a binding molecule for WAVE2 involved in spine morphogenesis, interacts with dysbindin-1. Although dysbindin-1, WAVE2 and Abi-1 form a ternary complex, dysbindin-1 promoted the binding of WAVE2 to Abi-1. RNA interference-mediated knockdown of dysbindin-1 led to the generation of abnormally elongated immature dendritic protrusions. The present results indicate possible functions of dysbindin-1 at the postsynapse in the regulation of dendritic spine morphogenesis through the interaction with WAVE2 and Abi-1.
