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Initiation of visual-guided random saccades and remembered saccades in parkinsonian patients with severe motor-fluctuations. 严重运动波动的帕金森病患者视觉引导随机扫视和记忆扫视的开始。
C Müller, S Wenger, L Fertl, E Auff

We studied the initiation of saccades to visual-guided random time and remembered targets in a group of nine Parkinsonian patients with severe motor fluctuations and in 9 age matched control subjects. In contrast to a marked skeletomotor improvement during the "on" condition, saccadic latencies for both visual-guided random saccades and remembered saccades were increased in the patients during the "on" condition compared to the "off" condition. This result of dissociation between skeletomotor and oculomotor function indicates that common concepts of saccadic initiation in parkinsonian patients do not hold true in patients with severe fluctuations since dopaminergic stimulation seems to increase saccadic latencies in these patients.

我们研究了9名患有严重运动波动的帕金森病患者和9名年龄匹配的对照组的扫视启动到视觉引导的随机时间和记忆目标。与“打开”状态下骨骼运动的显著改善相反,在“打开”状态下,与“关闭”状态相比,患者在视觉引导下的随机扫视和记忆扫视的跳眼潜伏期都有所增加。骨骼肌和动眼肌功能分离的结果表明,帕金森病患者眼跳肌启动的普遍概念在严重波动的患者中并不成立,因为多巴胺能刺激似乎增加了这些患者的眼跳肌潜伏期。
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引用次数: 17
Mitochondrial enzyme deficiencies in Down's syndrome. 唐氏综合症的线粒体酶缺乏。
J Prince, S Jia, U Båve, G Annerén, L Oreland

Defects in cytochrome oxidase (CO; complex 4) have recently been demonstrated in blood platelets and in brain tissue from patients with Alzheimer's disease (AD) with possible etiological implications. Because of pathogenetic similarities with AD, we have measured the activities of several mitochondrially localised enzymes in the blood platelets of individuals afflicted with trisomy-21 (Down's syndrome). The activities of monoamine oxidase, cytochrome oxidase, isocitrate dehydrogenase, and glutamate dehydrogenase were assayed in washed platelets from sixty caucasian, male and female control individuals (ages 18-60) and ten, young Down's Syndrome patients (ages 9-21). Significant reductions in the activities of monoamine oxidase, cytochrome oxidase, and isocitrate dehydrogenase were found. In all cases the average activities in Down's syndrome individuals were approximately two-thirds those of controls (DS/Controls = 0.68, 0.67, 0.64 respectively). The activity of the fourth enzyme studied, glutamate dehydrogenase, was found to be similar to controls. Results suggest that these reductions are a consequence of a generalised mitochondrial disturbance which may lie behind some pathogenetic aspect(s) of the disease.

细胞色素氧化酶缺陷;最近在阿尔茨海默病(AD)患者的血小板和脑组织中发现了复合物4,可能具有病因学意义。由于与AD的发病机制相似,我们测量了21三体(唐氏综合征)患者血小板中几种线粒体定位酶的活性。本文测定了60例白种人(18-60岁)和10例年轻唐氏综合征患者(9-21岁)的洗后血小板中单胺氧化酶、细胞色素氧化酶、异柠檬酸脱氢酶和谷氨酸脱氢酶的活性。单胺氧化酶、细胞色素氧化酶和异柠檬酸脱氢酶活性显著降低。在所有情况下,唐氏综合症个体的平均活动大约是对照组的三分之二(DS/对照分别= 0.68,0.67,0.64)。研究发现,第四种酶谷氨酸脱氢酶的活性与对照组相似。结果表明,这些减少是一个普遍的线粒体紊乱的结果,这可能是背后的一些致病方面的疾病。
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引用次数: 51
Effect of a selective MAO-A inhibitor (Ro 41-1049) on striatal L-dopa and dopamine metabolism: an in vivo study.
T Brannan, A Prikhojan, M D Yahr

We administered Ro 41-1049, an inhibitor of the enzyme monoamine oxidase type A (MAO-A) to rats and monitored extracellular catecholamine levels in the corpus striatum before and after the intraperitoneal (IP) administration of a bolus of L-dopa. Acute administration of Ro 41-1049 (1-50 mg/kg IP) produced a dose-dependent decrease in basal levels of the dopamine metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) and an increase in basal levels of dopamine. In rats treated with Ro 41-1049 (20 mg/kg IP), L-dopa administration (100 mg/kg IP) produced a greater increase in striatal levels of dopamine than it did in controls, while DOPAC and HVA formation was attenuated. We conclude that inhibition of central MAO-A activity promotes synaptic accumulation of dopamine following administration of pharmacological doses of L-dopa.

急性给药Ro 41-1049 (1-50 mg/kg IP)导致多巴胺代谢产物3,4-二羟基苯乙酸(DOPAC)和同型香草酸(HVA)基础水平呈剂量依赖性降低,多巴胺基础水平升高。在Ro 41-1049 (20 mg/kg IP)处理的大鼠中,左旋多巴(100 mg/kg IP)使纹状体多巴胺水平比对照组增加更多,而DOPAC和HVA的形成则减弱。
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引用次数: 1
Selective cortical decrease of high-affinity choline uptake carrier in Alzheimer's disease: an autoradiographic study using 3H-hemicholinium-3. 阿尔茨海默病中高亲和力胆碱摄取载体的选择性皮质减少:3h -钬-3放射自显影研究
R Rodríguez-Puertas, A Pazos, J J Zarranz, J Pascual

3H-hemicholinium-3 (3H-HC-3) binding, a marker of the presynaptic high-affinity choline uptake carrier (HACU), was measured by autoradiography in several brain regions of 17 Alzheimer's disease (AD) patients and of 11 matched controls. A significant decrease in the density of 3H-HC-3 binding sites was found in entorhinal cortex, hippocampus and layers I-III of the frontal cortex. By contrast, in the caudate-putamen the number of 3H-HC-3 binding sites in AD cases was comparable to that of control striata. These data concur with previous results using classical presynaptic markers and reflect the loss in the activity of HACU, and, hence, in the synthesis of acetylcholine, that selectively occurs in cortical areas of AD brains due to the degeneration of presynaptic cholinergic terminals arising from the basal forebrain. However, the relatively low mean reduction in HACU in cortical areas (-40%), together with the apparent indemnity of this marker in certain severely demented AD cases, suggest that AD dementia cannot be explained simply by the loss of presynaptic terminals originating in the basal forebrain. These data seem to be a good explanation for the poor response to cholinergic replacement in AD.

3H-HC-3结合是突触前高亲和力胆碱摄取载体(HACU)的标志物,通过放射自显影技术在17例阿尔茨海默病(AD)患者和11例匹配对照的几个脑区进行了测量。3H-HC-3结合位点在大鼠内嗅皮层、海马和额叶皮层I-III层的密度明显降低。相比之下,在AD病例的尾壳核中,3H-HC-3结合位点的数量与对照纹状体相当。这些数据与先前使用经典突触前标记物的结果一致,反映了HACU活性的丧失,从而反映了乙酰胆碱合成的丧失,这种丧失选择性地发生在阿尔茨海默病大脑皮层区域,原因是源于基底前脑的突触前胆碱能末梢的退化。然而,皮层区HACU相对较低的平均降低(-40%),以及在某些严重痴呆的AD病例中该标记物的明显补偿,表明AD痴呆不能简单地用起源于基底前脑的突触前终末的丧失来解释。这些数据似乎可以很好地解释AD患者对胆碱能替代的不良反应。
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引用次数: 24
A novel anticholinesterase THB013: biochemical and behavioural studies. 一种新型抗胆碱酯酶THB013:生化和行为研究。
A Adem, A H Mohammed, B Winblad, B E Henriksson

Clinical trials with tacrine (THA) have resulted in elevations of liver enzymes in Alzheimer patients that showed improvement. In an effort to minimize these side effects several THA analogues were synthesized. These analogues were compared to THA in biochemical as well as behavioural studies. In this study, the biochemical effects of THA and one of these analogs, THB 013, on plasma cholinesterase activity, cholinergic receptors as well as the effect of these drugs on spatial learning in adult rats were examined. THB 013 was, at lower concentration, more efficacious in inhibiting plasma cholinesterase as well as blocking the scopolamine induced disruption of spatial learning when administered 10 min before the scopolamine injection. It is possible that THB 013 with more potent cholinergic effects than THA might be useful in the treatment of Alzheimer's disease.

他克林(THA)的临床试验已导致阿尔茨海默病患者肝酶升高,表现出改善。为了尽量减少这些副作用,合成了几种THA类似物。这些类似物在生化和行为研究中与THA进行了比较。本研究考察了THA及其类似物thb013对成年大鼠血浆胆碱酯酶活性、胆碱能受体的生化影响以及对空间学习的影响。较低浓度的THB 013在东莨菪碱注射前10 min给予时,对血浆胆碱酯酶的抑制作用和对东莨菪碱引起的空间学习障碍的阻断作用更有效。THB 013具有比THA更强的胆碱能作用,可能有助于治疗阿尔茨海默病。
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引用次数: 3
Effects of trihexyphenidyl and L-dopa on brain muscarinic cholinergic receptor binding measured by positron emission tomography. 正电子发射断层扫描测定三己苯和左旋多巴对脑毒菌碱胆碱能受体结合的影响。
H Shinotoh, M Asahina, O Inoue, T Suhara, K Hirayama, Y Tateno

The effects of pharmacological intervention on brain muscarinic cholinergic receptor (mAChR) binding were assessed in seven patients with Parkinson's disease by positron emission tomography and carbon-11 labelled N-methyl-4-piperidyl benzilate ([11C]NMPB). [11C]NMPB was injected twice, approximately 2 hours apart, in each patient, to assess the effect of single doses of 4 mg of trihexyphenidyl (n = 5) or 400 mg of L-dopa with 57 mg of benserazide (n = 2) on the binding parameter of mAChRs (K3). There was a mean 28% inhibition of K3 values in the brain in the presence of trihexyphenidyl, which was assumed to reflect mAChR occupancy. No significant change in K3 was observed in the presence of L-dopa. This study demonstrates the feasibility of measuring mAChR occupancy by an anticholinergic medication with PET.

通过正电子发射断层扫描和碳-11标记的n-甲基-4-哌啶苄酯([11C]NMPB)评估了7例帕金森病患者的药物干预对脑毒毒碱胆碱能受体(mAChR)结合的影响。[11C]在每位患者中注射两次NMPB,间隔约2小时,以评估单剂量4mg三苯基(n = 5)或400mg左旋多巴加57mg苯肼(n = 2)对machr结合参数(K3)的影响。在三己苯基的存在下,大脑中K3值的平均抑制率为28%,这被认为反映了mAChR的占用。左旋多巴对K3无明显影响。本研究证明了用PET测定抗胆碱能药物占用率的可行性。
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引用次数: 13
Cerebrospinal fluid ferritin levels of patients with Parkinson's disease, Alzheimer's disease, and multiple system atrophy. 帕金森病、阿尔茨海默病和多系统萎缩患者的脑脊液铁蛋白水平。
M A Kuiper, C Mulder, G J van Kamp, P Scheltens, E C Wolters

Iron is believed to play a role in the pathogenesis of both Parkinson's disease (PD) and Alzheimer's disease (AD). We measured ferritin, which is considered to be the iron storage protein, in CSF of patients with PD, AD, and multiple system atrophy (MSA) as well as control subjects. We found a significant increase in CSF ferritin in AD compared with both PD and age-matched controls. No significant differences were found between PD patients with dementia (PDD) and non-demented PD patients. For non-demented PD patients a positive correlation between CSF ferritin and age was found. Our results may indicate that iron has a role in the pathophysiology of AD.

铁被认为在帕金森病(PD)和阿尔茨海默病(AD)的发病机制中发挥作用。我们测量了PD、AD和多系统萎缩(MSA)患者以及对照组脑脊液中的铁蛋白,铁蛋白被认为是铁储存蛋白。我们发现,与PD和年龄匹配的对照组相比,AD患者脑脊液铁蛋白显著增加。PD合并痴呆(PDD)患者与非痴呆PD患者之间无显著差异。对于非痴呆性PD患者,脑脊液铁蛋白与年龄呈正相关。我们的结果可能表明铁在阿尔茨海默病的病理生理中起作用。
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引用次数: 49
MPTP-induced behavioural and biochemical deficits: a parametric analysis. mptp诱导的行为和生化缺陷:参数分析。
A Fredriksson, T Archer

Two experiments were performed to study the parametric effects of long-term administration of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), as a functional model of parkinsonism in mice. The behavioural deficits induced by different doses of MPTP (5, 10, 20, 30 or 40 mg/kg, s.c., each injected on two occasions) at a 3-week or a 3-month treatment-testing interval were evidenced by significant reductions of spontaneous motor activity, from the 10 mg/kg dosages upwards at the 3-week interval and from 30-40 mg/kg at the 3-month interval. Significant dopamine (DA) reductions in the mouse striatum were obtained at these dose levels and intervals. The behavioural deficit of the 40 mg/kg dose (injected on two occasions) and tested at the 3-, 6-, 12-, 24- and 40-week intervals (separate as well as repeated testing groups) indicated marked and relatively comparable reductions of all three parameters of motor activity, locomotion, rearing and total activity. DA depletions were severe at all five test intervals. These results offer functional and neurochemical evidence that MPTP treatment produces permanent damage to the nigrostriatal motor system in mice.

两项实验研究了长期给药神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)作为小鼠帕金森病功能模型的参数效应。不同剂量的MPTP(5、10、20、30或40 mg/kg, s.c,每次注射两次)在3周或3个月的治疗-测试间隔中引起的行为缺陷,可以通过自发运动活动的显著减少来证明,从10 mg/kg剂量在3周间隔中增加,从30-40 mg/kg在3个月间隔中增加。在这些剂量水平和间隔下,小鼠纹状体中多巴胺(DA)显著减少。40 mg/kg剂量(注射两次)的行为缺陷,并在3周、6周、12周、24周和40周的间隔(单独和重复试验组)进行测试,表明运动活动、运动、饲养和总活动的所有三个参数都有明显的相对可比较的减少。在所有五个测试间隔中,DA消耗都很严重。这些结果为MPTP治疗对小鼠黑质纹状体运动系统产生永久性损伤提供了功能和神经化学证据。
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引用次数: 82
Role of D1 receptor mechanisms in the potentiation of motor responses to L-dopa and apomorphine by MK 801 in the reserpine-treated mouse. D1受体机制在利血平处理小鼠MK 801增强左旋多巴和阿波啡运动反应中的作用。
S Kaur, M S Starr, B S Starr

In 24 h reserpine-treated akinetic mice, locomotion was induced by the D1-selective agonist SKF 38393 (30 mg/kg IP), or by the mixed D1/D2 agonists L-dopa (150 mg/kg IP, plus benserazide 100 mg/kg IP) and apomorphine (0.5 mg/kg SC). The non-competitive NMDA receptor antagonist MK 801 (0.01-1.6 mg/kg IP) did not induce motor activity by itself, but potentiated the motor responses to L-dopa and apomorphine at roughly 10-fold lower doses than those which facilitated D1 responding. These data cast doubt on the notion that glutamate antagonists enhance the antiparkinsonian efficacy of mixed D1/D2 agonists solely through a D1 receptor mechanism.

利血平处理24 h后,D1选择性激动剂SKF 38393 (30 mg/kg IP)或D1/D2混合激动剂左旋多巴(150 mg/kg IP,加苯沙肼100 mg/kg IP)和阿波啡(0.5 mg/kg SC)诱导运动。非竞争性NMDA受体拮抗剂MK 801 (0.01 ~ 1.6 mg/kg IP)本身不诱导运动活动,但增强了左旋多巴和阿波啡的运动反应,其剂量比促进D1反应的剂量低约10倍。这些数据对谷氨酸拮抗剂仅通过D1受体机制增强混合D1/D2激动剂抗帕金森病疗效的观点提出了质疑。
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引用次数: 11
Neuron specific enolase in cerebrospinal fluid: a biochemical marker for neuronal degeneration in dementia disorders? 脑脊液中神经元特异性烯醇化酶:痴呆患者神经元变性的生化标志物?
K Blennow, A Wallin, R Ekman

Alzheimer's disease (AD) is the most common disease causing dementia. Today the clinical diagnosis of AD is made by way of exclusion, and no biochemical markers are available to assist the clinical diagnosis. We examined the potential of neuron-specific enolase (NSE) in cerebrospinal fluid (CSF) as a diagnostic marker for AD. NSE was determined with a monoclonal antibody two-site immunoradiometric assay (IRMA) in serum (S) and cerebrospinal fluid (CSF) samples from 45 patients with "probable Alzheimer's disease (AD)", 19 patients with vascular dementia (VAD) and 33 age-matched healthy individuals. There was no significant correlation between S-NSE and CSF-NSE, or between CSF/S albumin ratio and CSF-NSE, findings suggesting that the major portion of CSF-NSE is intrathecally produced and that analysis of CSF-NSE alone (without accompanying analysis of serum) is sufficient. CSF-NSE was significantly higher in the AD group (4.7 +/- 2.7 ng/mL; p < 0.0001) and in VAD group (4.5 +/- 2.5 ng/mL; p < 0.001) as compared with the control group (2.2 +/- 1.0 ng/mL), while it did not differ significantly between the AD and the VAD group. These findings suggest that CSF-NSE have a potential as a non-disease specific marker for the neuronal degeneration in dementia disorders.

阿尔茨海默病(AD)是最常见的导致痴呆症的疾病。目前对AD的临床诊断多采用排除法,没有生化标志物辅助临床诊断。我们研究了脑脊液(CSF)中神经元特异性烯醇化酶(NSE)作为AD诊断标志物的潜力。采用单克隆抗体双位点免疫放射测定法(IRMA)检测45例“疑似阿尔茨海默病(AD)”患者、19例血管性痴呆(VAD)患者和33例年龄匹配的健康人的血清(S)和脑脊液(CSF)样本中的NSE。S- nse与CSF- nse之间、CSF/S白蛋白比与CSF- nse之间无显著相关性,提示CSF- nse的主要部分是鞘内产生的,单独分析CSF- nse(不附带血清分析)就足够了。AD组CSF-NSE显著升高(4.7 +/- 2.7 ng/mL;p < 0.0001), VAD组(4.5 +/- 2.5 ng/mL;p < 0.001),与对照组(2.2 +/- 1.0 ng/mL)相比,AD组和VAD组之间无显著差异。这些发现提示CSF-NSE有潜力作为痴呆障碍中神经元变性的非疾病特异性标志物。
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引用次数: 48
期刊
Journal of Neural Transmission - Parkinson's Disease and Dementia Section
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