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Science:抗癌药物可能有助于治疗精神分裂症

据美国每日科学网报道,伦敦国王学院的彼得·吉斯领导的研究小组近日找到了影响精神分裂症的分子途径,并使用一种常用的抗癌药物MS-275成功地缓解了小鼠的精神分裂症症状。这项研究为研发精神分裂药物提供了新途径。

精神分裂症会导致幻觉、妄想和行为改变等长期心理症状,全球约2400万人受其影响,未经治疗的精神分裂患者有90%居于发展中国家。虽然人们普遍认为这是遗传和环境的共同作用,但其确切缘由尚未被知晓。目前精神分裂症的治疗方法,包括心理治疗如心理疗法、咨询、认知行为治疗和药物治疗,但很多抗精神病药物和绝大多数的安定药都有极大副作用。

吉斯团队在研究中首次发现,精神分裂症患者脑内的酶催化剂p35变少。正常的大脑发育部分是由Cdk5蛋白质的活化作用所保证的,而Cdk5的激活需要大脑中酶p35的存在,但精神分裂症患者大脑中酶p35比正常人少50%。

他们将小鼠的酶p35的含量减少到了相应的比例,然后对小鼠脑内的分子变化进行了监控。结果发现,p35的减少导致小鼠体内对维持神经连接有重要作用的突触蛋白质减少,并显露出神经分裂相关症状,如学习障碍、对感官刺激无法作出回应,表现出认知功能障碍等。

研究还发现,p35的减少引起的分子变化与抗癌药物MS-275的药物靶点相一致。MS-275不仅处理了小鼠的分子变化,而且减少了其与精神分裂症相关的症状。了解这一信号通路及p35减少所引起的后果,对精神分裂症潜在的治疗方法有重要指导作用。

吉斯称,该研究成果鼓舞了未来治疗精神分裂症患者的药物研发,有助于精神分裂症的治疗。

抗癌药物可能有助于治疗精神分裂症

 

 

英文原文报道:

Cancer Drugs May Help Treatment of Schizophrenia

Researchers have revealed the molecular pathway that is affected during the onset of schizophrenia and successfully alleviated symptoms of the illness in mice, using a commonly used cancer drug.

The research, published online in the journal Brain, is from a group led by Professor Peter Giese at King's College London, and offers new avenues for drug discovery.

Schizophrenia is one of the most common serious mental health conditions in the UK, and affects about 24 million people worldwide. The illness is a long-term mental health condition that causes a number of psychological symptoms, including hallucinations and delusions as well as behaviour changes. The exact cause of the illness is unknown, although it is generally believed to be a combination of genetic and environmental factors.

According to the World Health Organization, 90% of people with untreated schizophrenia are in developing countries. Current treatments for schizophrenia include both psychological treatments such as psychotherapy, counselling or cognitive behaviour therapy and/or medication. However, many of the antipsychotic drugs or major tranquillisers used to treat or manage the illness have very bad side-effects.

Professor Giese, based at the Institute of Psychiatry at King's, said: 'For the first time we have found that an enzyme activator called p35 is reduced in patients with schizophrenia and moreover, modelling this reduction in mice led to cognitive impairment typical for this disease. This gives us a better understanding of the changes that occur in the brain during the onset of schizophrenia.'

Proper brain development is ensured, in part, by the activation of a protein in the brain called Cdk5. The activation of Cdk5 requires the presence of an enzyme in the brain, called p35. The research found that in human post-mortem brains, there was approximately 50% less p35 in the brains of patients who had suffered from schizophrenia.

These molecular changes were then modelled and monitored in mice that had been modified to contain a comparable reduction in the p35 enzyme. As a result of this reduction in p35, the mice showed a reduction in synaptic proteins -- important in maintaining neural connections -- and displayed symptoms associated with schizophrenia, including learning impairments and inability to react to sensory stimuli.

Understanding this signalling pathway and the impact of low levels of p35, is important in finding potential future treatments for the disease.

Professor Giese continues: 'We noted that the reduction in p35 affects the same molecular changes targeted by a cancer drug called MS-275, so we administered this drug to the mice. We were excited to find that MS-275 not only addressed the molecular changes but also alleviated the symptoms associated with schizophrenia.'

He concludes: 'Our findings encourage the future exploration of these types of drugs for treating impaired cognition in schizophrenia.'

The research was funded by the Medical Research Council UK (MRC), the National Institutes of Health (USA), the Boehringer Ingelheim Fonds, Germany and the Deutsche Forschungsgemeinshaft.

 

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