有效防治高血压和糖尿病是预防痴呆的关键

老年性痴呆主要包括阿尔茨海默病(AD)、血管性痴呆(VD)和混合性痴呆(MD).随着对痴呆相关疾病认识的逐渐深入,痴呆危险因素、病因和发病机制日益受到关注.     

应加强对血管性认知损害的防与治

在老年期痴呆中,血管性痴呆(VaD)和阿尔茨海默病(AD)是最为常见的两种类型。而血管性痴呆与阿尔茨海默病相比,病因较明确,患者多有脑卒中病史,表现为波动性病程、阶梯式恶化,而且相对可干预治疗,疗效和预后相对较好。因此,对于血管性痴呆患者早期发现、早期诊断即显得尤为重要。随着对认知功能障碍形式、严重程度和脑组织损害等方面的深入研究,发现以阿尔茨海默病为模式的血管性痴呆诊断标准存在明显缺陷。为此,     

皮质下血管性痴呆与脑白质疏松症关系的研究

随着社会的老龄化，痴吊患呈逐年递增的趋势，血管生痴呆（vascular dementia,VD)的发病率仅次于阿尔茨海默病（Alzheimer disease,AD)，而皮质下血管性痴呆是血管性痴呆的亚型之一，占血管性痴呆的75.92%；在皮质下血管性痴呆患中，脑白质疏松症（leukoraiosis，     

血塞通联合尼莫地平治疗轻中度血管性痴呆临床观察

血管性痴呆(vascular dementia,VD)又称多发梗死性痴呆,VD与阿尔茨海默病(Alzheimer disease,AD)是老年期痴呆的两个主要类型。随着人群老龄化及脑血管发病率逐年上升,血管性痴呆己成为仅次于阿尔茨海默病最常见的痴呆类型[1-2]。本文应用血塞通粉剂联合尼莫地平治疗轻中度血     

阿尔茨海默病与血管性危险因素

阿尔茨海默病(Alzheimer disease,AD)是一种多因素致病疾病,涉及遗传、环境和社会心理等诸多方面以及不同因素之间复杂的相互作用。研究结果显示,血管性危险因素不仅与认知损害和血管性痴呆(vascular dementia,VD)有关,     

血管性痴呆患者神经精神症状的临床分析

目的 了解血管性痴呆患者的神经精神症状特点.方法 采用神经精神科问卷、简易智能状态检查量表和Hachinski缺血评分量表,分别评价血管性痴呆、脑卒中后非痴呆、阿尔茨海默病和正常老年人群的神经精神症状.结果 与正常对照组比较,血管性痴呆组患者在妄想、幻觉、激越、抑郁和(或)心境恶劣、情感淡漠、易激惹和(或)不稳定、迷乱的动作行为等调查内容和神经精神科问卷总评分,差异有统计学意义(P＜0.05或P＜0.01);阿尔茨海默病组伴妄想者多于血管性痴呆组,组间差异有统计学意义(P＜0.01).血管性痴呆不同严重程度组之间比较,幻觉、焦虑、情感淡漠、易激惹和(或)不稳定、迷乱的动作行为等调查项目达到统计学意义(P＜0.05或P＜0.01),且随病情的逐渐加重而症状更为明显.结论 血管性痴呆和阿尔茨海默病患者存在多种相似的神经精神症状,中至重度血管性痴呆患者表现为以情绪和情感障碍为主的神经精神症状.     

血管性痴呆的遗传学机制研究进展

血管性痴呆是仅次于阿尔茨海默病的第二大痴呆类型,其发病率逐年增加。血管性痴呆的发病机制尚未明确,目前认为其发病是环境和基因等多种复杂因素共同作用的结果。随着基因组测序技术的发展,近年来大量文献报道了与血管性痴呆相关的基因多态性位点。本文综述了与血管性痴呆发病的遗传因素,总结了目前已知与血管性痴呆发病相关的遗传学研究进展。     

血管性痴呆及其治疗

在老年期痴呆中 ,血管性痴呆和阿尔茨海默病是两种主要疾病 ,其中前者有较明确的病因和危险因素 ,在一定程度上可以预防 ,而且治疗途径广泛 ,本文从多个角度阐述血管性痴呆的治疗     

中风与神经疾病杂志2008年第25卷文题索引

(按汉语拼音字母顺序排列)A阿尔茨海默病Alzheimer Disease病因研究现状(4):510Alzheimer病与血管性痴呆患者认知功能对照研究(6):710阿尔茨海默病患者扣带回后部各向异性与葡萄糖代谢关系研究(4):398PLAU基因单体型与晚发性阿尔茨海默病的相关研究(3):289心血管危险因素对阿尔     

轻度认知障碍与无痴呆型血管性认知障碍患者的神经心理学特征

阿尔茨海默病（AD）和血管性痴呆（vascular dementia，VD）是临床常见的老年期痴呆类型。虽然长期以来受到广泛关注．但对其治疗收效甚微．近年逐渐将研究重点转向对其早期阶段的干预治疗。在这一临床需要下，针对阿尔茨海默病和血管性痴呆分别提出了轻度认知障碍（mild cognitive impairment，MCI）和血管性认知障碍（vascular cognitive impairment，VCI）的概念，力求对患者进行早期识别和干预，以延缓甚至阻止痴呆的发生、发展。     

Pregabalin effect on steady-state pharmacokinetics of carbamazepine, lamotrigine, phenobarbital, phenytoin, topiramate, valproate, and tiagabine

By reducing neuronal excitability through selective binding to the α(2)δ subunit of voltage-dependent calcium channels, pregabalin effectively treats epilepsy, chronic pain, and anxiety disorders. To evaluate if pregabalin coadministration affects pharmacokinetics of other antiepileptic drugs, population pharmacokinetic analyses using NONMEM software were performed on data from three epilepsy trials involving seven antiepileptic drugs with pregabalin as add-on therapy. Results demonstrated that pregabalin did not alter the steady-state plasma concentrations of carbamazepine, lamotrigine, phenobarbital, phenytoin, tiagabine, topiramate, and valproate. Furthermore, the small percent change in the population estimate of antiepileptic drug plasma clearance values (-2% to +7%) suggests that pregabalin coadministration exerted no significant effect on the pharmacokinetics of these antiepileptic drugs, with the possible exception of tiagabine (+34.9%). These findings are in agreement with those of previously published reports. A further clarification study is necessary for tiagabine. In conclusion, it appears that pregabalin can be coadministered with other antiepileptic drugs without concern for significantly altering their pharmacokinetic profiles.     

Consecutive Gas Chromatographic Determination of Phenytoin, Phenobarbital, Primidone, Phenylethylmalondiamide, Carbamazepine, Trimethadione, Dimethadione, Ethosuximide, and Valproate from the Same Serum Specimen

A quantitative gas-liquid chromatographic procedure is described for the consecutive determination of phenytoin, phenobarbital, primidone, phenylethylmalondiamide, carbamazepine, trimethadione, dimethadione, ethosuximide and valproate from a single serum specimen of 1.2 ml. After extraction from serum by two different procedures, the anticonvulsants are chromatographed without further purification on a 3% OV 17 column either with or without derivative formation by means of "on-column" methylation. Multiple internal standards are employed in order to enhance the reproducibility of drug-concentration measurement.     

Mass spectrometric identification of Cu, Zn, Fe, Co, Mn, Mg, and Pb in mammalian brain.

Combining the techniques of thin-layer chromatography (TLC) and mass spectrometry, we unambiguously identified the trace metals Cu, Zn, Fe, Pb, Mn, Co, and Mg in the brain of a female human who had no evidence of any pathologic disease in the central nervous system, and in brains from mouse, rat, guinea pig, and rabbit. These trace metals were also found in anatomic regions of human brain: cortex (gray), cortex (white), caudate nucleus, putamen, hippocampus, and thalamus, and in anatomic regions of rat brain: hypothalamus, cerebellum, stem striatum, and "the rest." The metals were characterized from the color and Rf values of their tetraphenylporphyrin chelates on TLC and from the mass and pattern of molecule ion cluster of the mass spectrum. The unexpected presence of lead in the brain is discussed.     

中国汉族人群SCA1、2、3、6、7、8、10、12、17亚型和齿状核-红核-苍白球-路易体萎缩亚型频率分布

目的 研究中国汉族人群中脊髓小脑性共济失调(SCAs)不同基因亚型的频率分布.方法 运用聚合酶链反应、变性聚丙烯酰胺凝胶电泳、Southern blot、T载体克隆重组DNA技术结合直接测序等技术对559例临床诊断为SCA的患者(363例常染色体显性遗传先证者,196例散发患者)进行了SCA1、SCA2、SCA3/MJD、SCA6、SCA7、SCA8、SCA10、SCA12、SCA17和齿状核-红核-苍白球-路易体萎缩(DRPLA)致病基因多核苷酸病理重复突变检测分析.结果 在363个常染色体显性遗传的SCA(AD-SCA)家系中,发现有15个SCA1家系(4.13%),26个SCA2家系(7.16%),187个SCA3/MJD家系(51.52%),6个SCA6家系(1.65%),7个SCA7家系(1.93%),1个SCA12家系(0.28%)和1个SCA17家系(0.28%),120个SCA家系未明确基因分型(33.06%);在196例散发SCA患者中,发现有2例SCAI患者(1.02%),3例SCA2患者(1.53%),15例SCA3/MJD患者(7.65%),3例SCA6患者(1.53%),173例SCA患者未明确基因分型(88.27%);未发现SCA8、SCA10和DRPLA型患者.结论 在中国汉族人群中SCA3/MJD为最常见的SCA亚型,其次为SCA2、SCA1、SCA7和SCA6,SCA12和SCA17比较少见,SCA8、SCA10和DRPLA罕见,SCA17亚型为国内首次报道.部分AD-SCA家系存在其他致病基因的作用,大部分散发SCA患者除遗传因素外还存在其他致病因素.