Psychosis is a common non-motor symptom of Parkinson’s disease whose pathogenesis remains poorly understood. Parkinson’s disease in conjunction with psychosis has been shown to induce injury to extracorticospinal tracts as wel as within some cortical areas. In this study, Parkinson’s disease patients with psychosis who did not receive antipsychotic treatment and those without psychosis underwent diffusion tensor imaging. Results revealed that in Parkinson’s disease patients with psychosis, damage to the left frontal lobe, bilateral occipital lobe, left cingulated gyrus, and left hippocampal white-matter fibers were greater than damage to the substantia nigra or the globus pal idus. Damage to white-matter fibers in the right frontal lobe and right cingulate gyrus were also more severe than in the globus pal idus, but not the substantia nigra. Damage to frontal lobe and cingulate gyrus white-matter fibers was more apparent than that to occipital or hippocampal fiber damage. Compared with Parkinson’s disease patients without psychosis, those with psychosis had significantly lower fractional anisotropy ratios of left frontal lobe, bilateral occipital lobe, left cingu-lated gyrus, and left hippocampus to ipsilateral substantia nigra or globus pal idus, indicating more severe damage to white-matter fibers. These results suggest that psychosis associated with Par-kinson’s disease is probably associated with an imbalance in the ratio of white-matter fibers be-tween brain regions associated with psychiatric symptoms (frontal lobe, occipital lobe, cingulate gyrus, and hippocampus) and those associated with the motor symptoms of Parkinson’s disease (the substantia nigra and globus pal idus). The relatively greater damage to white-matter fibers in psychiatric symptom-related brain regions than in extracorticospinal tracts might explain why psy-chosis often occurs in Parkinson’s disease patients.

Because neurons are susceptible to oxidative damage and thioredoxin reductase 1 is extensively distributed in the central nervous system and has antioxidant properties, we speculated that the enzyme may be involved in the pathogenesis of Parkinson’s disease. A Parkinson’s disease model was produced by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine into C57BL/6 mice. Real-time reverse transcription-PCR, western blot analysis and colorimetric assay showed that the levels of thioredoxin reductase 1 mRNA and protein were decreased, along with a significant reduction in thioredoxin reductase activity, in the midbrain of Parkinson’s disease mice compared with normal mice. Immunohistochemical staining revealed that the number of thioredoxin reductase 1-positive neurons in the substantia nigra pars compacta of Parkinson’s disease mice was significantly decreased compared with normal mice. These experimental findings suggest that the expression of thioredoxin reductase 1 in the substantia nigra pars compacta of Parkinson’s disease mice is significantly decreased, and that the enzyme may be associated with disease onset.

大鼠尾核多巴胺受体抑制对黑质升压作用的影响

-纹状体多巴胺系统是中枢多巴胺系统的重要组成成分.资料表明,谷氨酸钠微量注入及电刺激黑质(substantia nigra,SN)均可使血压升高,幼年自发性高血压大鼠(spontaneously Hypertensive Rat,SHR)脑室注射6-羟多巴胺使额皮质和尾状核中DA下降,并能削弱SHR高血压的发展,电解损毁黑质使SHR血压升高延迟,这提示黑质DA能神经元可能通过中枢机制发挥其升压作用,并可推测黑质-纹状体DA系统在高血压发展中起作用.

帕金森病患者36例免疫状态改变的分析

Background: Parkinson' s disease (PD) is a degeneration disease with the main lesion being in the substantia nigra and corpus striatum. The current treatment is still dopamine preparation, but this cannot prevent the progress of the disease. The mechanism is believed to be related to immunological factors.

低剂量MPTP致雌鼠黑质听觉P50诱发电位动态变化的实验研究

近年来有研究[1]认为帕金森病(Parkinson's Disease,PD)的高发病率可能与杀虫剂的广泛使用,即环境因素有关,而杀虫剂内含具有致多巴胺神经元损伤死亡的神经毒素1-甲基-4苯基-1,2,3,6-四氢吡啶(MPTP).大量研究[2,3]采用MPTP在大鼠、猴等动物上模拟制备PD模型,其症状、生物化学反应和神经病理改变与PD十分相似.