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1.
目的探讨盐酸多奈哌齐治疗阿尔茨海默病的临床效果。方法选取2016年2月至2018年12月在徐州市第一人民医院治疗的62例老年痴呆患者为研究对象,分为对照组与观察组,每组31例。对照组给予常规治疗;观察组在常规治疗基础上给予盐酸多奈哌齐治疗。比较两组患者的临床疗效、日常生活活动评估量表(ADL)及简易智力状态检查量表(MMSE)评分、不良反应发生情况。结果观察组患者的治疗总有效率(96.77%,30/31)明显高于对照组(77.42%,24/31),差异有统计学意义(P0.05);观察组不良反应发生率(6.45%,2/31)低于对照组(25.81%,8/31),差异有统计学意义(P0.05);观察组ADL评分、MMSE评分明显高于对照组,差异有统计学意义(P0.05)。结论老年痴呆患者采取盐酸多奈哌齐治疗可改善患者精神状态,提高其日常生活能力,且安全性高,具有推广价值。  相似文献   

2.
盐酸多奈哌齐治疗阿尔茨海默病的临床观察   总被引:1,自引:0,他引:1  
近年来许多研究表明阿尔茨海默病 (AD)脑中乙酰胆碱浓度降低会导致认知功能障碍 ,盐酸多奈哌齐 (Donepezilhy drochloride)是一种具有高度选择性、长效的、可逆性的乙酰胆碱酯酶抑制剂 ,胆碱酯酶的基本作用是降解脑中乙酰胆碱。我们应用盐酸多奈哌齐治疗AD 2 4例收到较满意的效果 ,报告如下。1 资料与方法1.1 一般资料 根据美国NINCDS ADRDA可能的AD诊断标准和DSM IV (1994)AD诊断标准 ,简易智能状态检查(MMSE)总分为 12~ 2 4的轻至中度痴呆病人 ,年龄≥ 5 5岁 ,全部患者皆经脑CT…  相似文献   

3.
目的 探讨盐酸多奈哌齐联合阿托伐他汀钙治疗轻、中度阿尔茨海默病的临床疗效和安全性.方法 将208例轻、中度阿尔茨海默病患者随机分为两组,联合组口服盐酸多奈哌齐联合阿托伐他汀钙治疗,对照组口服盐酸多奈哌齐治疗.观察6个月.治疗前后采用简易精神状态量表评定认知功能,日常生活功能量表评定行为功能,检测血脂水平的变化,随时记录治疗过程中出现的不良反应.结果 治疗后联合组总胆固醇、低密度脂蛋白水平均较治疗前显著下降(P<0.01),高密度脂蛋白水平较治疗前显著升高(P<0.01);对照组治疗后各项指标均无显著变化.两组简易精神状态量表评分均较治疗前显著升高(P<0.01),联合组较对照组升高更显著(P<0.01);日常生活功能量表评分均较治疗前显著下降(P<0.01),联合组较对照组下降更显著(P<0.05).两组不良反应均轻微.结论 盐酸多奈哌齐联合阿托伐他汀钙治疗能显著改善轻、中度阿尔茨海默病患者的认知功能和日常生活能力,安全性高,依从性好,优于单用盐酸多奈哌齐治疗.  相似文献   

4.
背景:盐酸多奈哌齐治疗阿尔茨海默病(Alzheimer disease,AD)受到临床关注,但其对认知功能及日常生活能力的改善是否有显著作用?目的:探讨盐酸多奈哌齐改善AD患者认知功能及日常生活能力的疗效。评价盐酸多奈哌齐治疗AD患者的有效性及安全性。设计:以诊断为依据的自身对照研究。地点和对象:1998-01/2001-03华中科技大学同济医学院附属梨园医院门诊和住院32例AD患者。干预:采用盐酸多奈哌齐5mg/d治疗16周。治疗前后用简易智能精神状态检查量表(MMSE)、阿尔茨海默病评定量表(the Alzheimer disease assessment scale。ADAS)及Blessed-Roth Scale痴呆量表评定患者认知功能及痴呆严重程度、精神行为异常和日常生活自理能力。并进行安全性评价。主要观察指标:①AD患者治疗前后MMSE,ADAS,Blessed-Roth Scale痴呆量表评分。②AD患者治疗期间不良反应。结果:盐酸多奈哌齐治疗后,患者MMSE评分较治疗前平均提高(4.1&;#177;1.1)分(P&;lt;0.01),ADAS认知部分改善(5.1&;#177;1.3)分(P&;lt;0.05);Blessed-Roth日常生活自理能力改善(1.2&;#177;0.5)分(P&;lt;0.05);ADAS韵非认知行为部分减少(3.7&;#177;0.9)分,(P&;lt;0.05),2例(6%)出现轻度副作用。结论:盐酸多奈哌齐治疗AD有较好的疗效并安全性好,副作用小。  相似文献   

5.
目的:探究采用盐酸多奈哌齐联合奥拉西坦治疗阿尔茨海默病患者的效果。方法:选取2017年12月~2018年12月收治的96例阿尔茨海默病患者,根据治疗方案不同分为观察组和参照组,各48例。参照组采用盐酸多奈哌齐治疗,观察组采用盐酸多奈哌齐联合奥拉西坦治疗,对比两组临床疗效,治疗前后智力状况、痴呆病理行为、日常生活能力及不良反应发生情况。结果:治疗12周后,观察组总有效率91.67%高于参照组的75.00%(P<0.05);观察组日常生活能力量表、简易智能状态量表评分高于参照组,痴呆病理行为量表评分低于参照组(P<0.05);观察组不良反应发生率14.58%与参照组的10.42%比较,差异无统计学意义(P>0.05)。结论:采用盐酸多奈哌齐联合奥拉西坦治疗阿尔茨海默病疗效确切,可有效提升患者日常生活能力及智力水平,改善病理行为障碍,不良反应少。  相似文献   

6.
目的 探究益生菌制剂联合多奈哌齐对中重度阿尔茨海默病(AD)患者临床疗效及炎症因子的影响。方法 选择80例中重度AD患者为研究对象,采用随机数字表法将患者分为观察组和对照组,各40例。对照组给予多奈哌齐治疗,观察组给予益生菌制剂联合多奈哌齐治疗。采用简易精神状态量表(MMSE)评分评定治疗疗效,采用AD评估量表认知次量表(ADAS-Cog)及AD评估量表日常生活能力次量表行为量表(ADAS-ADL)评价患者治疗前后的认知功能及日常生活能力,比较两组炎症因子[肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)]、氧化应激指标[超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛]及肠道菌群分布情况,并统计治疗不良反应发生情况。结果 两组治疗总有效率(95.00%vs 90.00%)比较,差异无统计学意义(χ2=0.72,P>0.05);治疗后,观察组患者MMSE及ADAS-ADL评分均高于对照组,ADAS-Cog评分低于对照组(t分别=2.92、2.37、-2.78,P均<0.05);观察组治疗后TNF-α...  相似文献   

7.
盐酸多奈哌齐治疗阿尔茨海默病的临床疗效和安全性观察   总被引:2,自引:0,他引:2  
目的探讨盐酸多奈哌齐对阿尔茨海默病(Alzheimer's disease,AD)治疗的有效性及安全性。方法32例AD患者随机分为对照组、治疗组,治疗组给予盐酸多奈哌齐治疗24周,对照组只给予维生素E治疗24周。治疗前后采用阿尔茨海默病评定量表的认知次级量表(ADAS-cog)和简易智能精神状态检查量表(MMSE)及日常生活能力量表(ADL)进行疗效评定。结果治疗组治疗16周后较治疗前ADAS-cog、MMSE及ADL评分有明显改善,治疗组治疗后16周末和治疗后24周末,ADAS-cog评分分别为20.6±6.5(P<0.05)和19.7±6.9(P<0.05),MMSE评分分别为23.0±2.6和27.1±2.9(P<0.01)及ADL评分分别为25±7和23±8(P<0.01),而对照组患者评分无明显改变,治疗患者无明显药物不良反应。结论盐酸多奈哌齐可以安全地用于治疗阿尔茨海默病。  相似文献   

8.
目的:探究盐酸多奈哌齐治疗阿尔茨海默病的临床治疗效果.方法:抽选2017年7月至2019年7月在本院接受诊治的阿尔茨海默病患者,人数为72例,基于单盲分组法将患者分为两组,每组例数为36例,参照组予以患者常规疗法,研究组在常规治疗的基础上联合盐酸多奈哌齐对患者施以治疗,对两组患者的治疗效果、生活能力、痴呆情况以及不良反...  相似文献   

9.
目的:分析尼莫地平联合多奈哌齐治疗阿尔茨海默病的临床疗效。方法:选择我院2013年9月~2017年3月收治的120例阿尔茨海默病患者为研究对象,按就诊时间的先后分为三组。尼莫地平组仅给予尼莫地平口服,40 mg/次,3次/d;多奈哌齐组仅给予多奈哌齐治疗,首次用药5 mg/d,睡前服用,若无严重不良反应,1个月后剂量增加至10 mg/d,否则恢复至5 mg/d;联合用药组以尼莫地平联合多奈哌齐治疗,两种药物剂量和用法同前两组。三组患者均治疗3个月,随访6个月。观察各组患者治疗前后智能状态(MMSE)、日常生活能力量表(ADL)、AD评估量表认知分量表(ADAS-Cog)评分,同时观察患者不良反应发生情况。结果:治疗前三组患者MMSE、ADAS-cog、ADL评分比较差异均无统计学意义(P0.05)。治疗6个月时三组患者MMSE、ADAS-cog、ADL评分与治疗前比较差异均有统计学意义(P0.05),但联合组各项数据改善均明显优于其他组,差异有统计学意义(P0.05)。结论:多奈哌齐联合尼莫地平治疗阿尔茨海默病在一定程度上会产生协同作用,且不良反应未见增加。两种药物联用治疗阿尔茨海默病对患者认知、智力及日常生活能力改善作用明显,且疗效明显优于单一用药,安全有效,值得推广。  相似文献   

10.
选取136例阿尔茨海默病患者,分为观察组及对照组各68例,对照组给予单服多奈哌齐,观察组给予尼莫地平联合多奈哌齐。对两组患者疗效及不良反应发生情况进行比较分析。结果治疗后观察组ADAS-Cog和MMSE评分情况均明显优于对照组(P〈0.05);两组不良反应发生率差异无统计学意义(P〉0.05)。尼莫地平联合多奈哌齐治疗AD的临床疗效优于单用多奈哌齐,且不良反应发生率低,值得推广。  相似文献   

11.
目的:对比分析阿尔茨海默病与帕金森病痴呆的认知功能及精神行为的异同点。方法:选取本院接诊的阿尔茨海默病患者52例(AD组)和帕金森病痴呆患者32例(PDD组),采用相关量表(CDR、MMSE、MoCA、CDT、CNPI)评估两组患者的认知功能、精神行为症状,总结各组的认知功能及精神行为特征。结果:两组的痴呆严重程度、MMSE、MoCA总分比较,差异均无统计学意义(P0.05)。与AD组相比,PDD组的CDT评分更低、CNPI评分更高(P0.05)。AD组与PDD组在命名、注意、语言、抽象思维、定向维度的评分比较,差异均无统计学意义(P0.05)。与PDD组相比,AD组的视空间/执行功能评分更高,记忆维度、延迟记忆维度评分更低(P0.05)。两组的妄想、欣快、脱抑制、异常运动行为、睡眠夜间行为、食欲进食障碍发生率比较,差异均无统计学意义(P0.05)。与AD组相比,PDD组的幻觉、激越、抑郁发生率更高,焦虑、淡漠、易激惹发生率更低(P0.05)。结论:相比AD,PDD的执行功能和视空间功能损伤更为严重,PDD的精神行为症状以幻觉、激越、抑郁居多,而AD多见焦虑、淡漠、易激惹。  相似文献   

12.
ObjectiveThis case‐control study was designed to compare the composition of the predominant oral bacterial microbiome in Alzheimer''s disease (AD) and control group.SubjectA total of 30 adult participants (15 AD and 15 healthy individuals) were entered in this study. The composition of oral bacterial microbiome was examined by quantitative real‐time polymerase chain reaction (qPCR) using bacterial 16S rDNA gene. The levels of systemic inflammatory cytokines in both groups were assessed using enzyme‐linked immunosorbent assays (ELISA).ResultsThe loads of Porphyromonas gingivalis, Fusobacterium nucleatum, and Prevotella intermedia were significantly more abundant in the AD compared to the control group (< 0.05). Although Aggregatibacter actinomycetemcomitans and Streptococcus mutans were relatively frequent in the AD group, no significance difference was observed in their copy number between two groups. Although the concentrations of IL‐1, IL‐6, and TNF‐α were higher in the AD group, there was a significant difference in their levels between the two groups (p < 0.05). Finally, there was a significant relationship between increased number of pathogenic bacteria in oral microbiome and higher concentration of cytokines in patient''s blood.ConclusionOur knowledge of oral microbiome and its exact association with AD is rather limited; our study showed a significant association between changes in oral microbiome bacteria, increased inflammatory cytokines, and AD.  相似文献   

13.
《Annals of medicine》2013,45(2):99-102
This study examined the relation between amyloid fibrils and senile plaques in brains of patients with Alzheimer's disease. All the senile plaques contained some amyloid fibrils, which seemed to be produced in the basement membranes of capillary endothelial cells and projecting into surrounding parenchyma. Even when amyloid fibrils could not be seen in senile plaques using light microscopy, at least one degenerate capillary containing amyloid fibrils was found when serial sections were examined by electron microscopy. Amyloid fibrils consisted of hollow rods and were composed of filaments arranged as a tightly coiled helix, each turn comprising five globular subunits. Many capillaries and microvessels showed degenerative changes. Many terminal arterioles had smooth muscle cells with an irregular shape and arrangement, often showing a series of focal constrictions.

The findings suggest that the capillary degeneration with the formation of amyloid fibrils may be a primary change in the genesis of senile plaques. Furthermore, degenerative changes in the microvessels may also be an important factor in the loss of neurons in the brain of subjects with Alzheimer's disease.  相似文献   

14.
Large numbers of neuritic plaques (NP), largely composed of a fibrillar insoluble form of the β-amyloid peptide (Aβ), are found in the hippocampus and neocortex of Alzheimer''s disease (AD) patients in association with damaged neuronal processes, increased numbers of activated astrocytes and microglia, and several proteins including the components of the proinflammatory complement system. These studies address the hypothesis that the activated complement system mediates the cellular changes that surround fibrillar Aβ deposits in NP. We report that Aβ peptides directly and independently activate the alternative complement pathway as well as the classical complement pathway; trigger the formation of covalent, ester-linked complexes of Aβ with activation products of the third complement component (C3); generate the cytokine-like C5a complement-activation fragment; and mediate formation of the proinflammatory C5b-9 membrane attack complex, in functionally active form able to insert into and permeabilize the membrane of neuronal precursor cells. These findings provide inflammation-based mechanisms to account for the presence of complement components in NP in association with damaged neurons and increased numbers of activated glial cells, and they have potential implications for the therapy of AD.  相似文献   

15.
ObjectivePoor oral health, mainly tooth loss, has been suggested to pose a risk factor for Alzheimer''s disease (AD). The nature of this relationship can be explained by mastication deficit and nutritional status. Also, the influence of nutritional parameters on cognitive impairment has been documented. The aim of this study was to investigate whether poor dental status and nutrition habits can be potential separate or associated risk factors for development of the AD.MethodsThe study sample included 116 patients with AD and 63 controls. Sociodemographic variables were investigated as factors potentially associated with AD. Dental examination included recording the number of natural teeth, presence of fixed or removable dentures, and the number of functional tooth units (FTUs). Nutritional status analysis included qualitative nutrition information, body mass index, serum albumin level, food consistency, and need for assistance in feeding. Regression analysis was used to investigate the predictors for development of AD.ResultsVariables with significant differences between groups, which were analyzed by using the binary regression analysis, were marital status, residence, number of total FTUs (no matter whether the contacts were between natural teeth or dentures), eating meat/fish and fruits/vegetables, food consistency, and serum albumin level. Logistic regression analysis showed that being single/widowed/divorced, eating more meat/fish or fruit/vegetable, eating blended/mashed/liquid food, having low levels of serum albumin, and having less FTUs were significant predictors for developing dementia.ConclusionHaving fewer occlusal contacts, consumption of soft food, and lower serum albumin levels can be considered as associated risk factors for AD.  相似文献   

16.
目的:探讨重复经颅磁刺激(rTMS)联合多奈哌齐对轻、中度阿尔茨海默病(AD)患者的疗效及安全性。方法:52例轻、中度AD患者随机分为研究组和对照组各26例,研究组采用rTMS联合多奈哌齐治疗,对照组单用多奈哌齐治疗。2组患者分别在治疗前及治疗4周、8周、12周后进行阿尔茨海默病评定量表认知分量表(ADASCog)、简易精神状态检查量表(MMSE)、日常生活能力量表(ADL)评定,于治疗前及治疗12周后进行事件相关电位P300检测。通过实验室检查和临床观察评定不良反应。结果:治疗4周后,研究组ADAS-Cog、MMSE、ADL评分与治疗前比较差异无统计学意义,治疗8及12周后,研究组ADAS-Cog及ADL评分较治疗前呈持续下降(P0.05),MMSE评分较治疗前持续增高(P0.05);对照组治疗4及8周后ADAS-Cog、MMSE、ADL评分与治疗前比较均差异无统计学意义,治疗12周后ADAS-Cog评分、ADL评分较治疗前明显下降(P0.05)、MMSE评分较治疗前明显增高(P0.05)。组间比较,治疗4周、8周后2组各量表评分差异均无统计学意义,治疗12周后研究组ADAS-Cog评分、ADL评分明显低于对照组(P0.05)、MMSE评分明显高于对照组(P0.05)。治疗12周后,2组P300潜伏期均较治疗前明显缩短(P0.05)、波幅明显升高(P0.05);组间比较,研究组P300潜伏期明显低于对照组(P0.05)、波幅明显高于对照组(P0.05)。结论:rTMS辅助多奈哌齐治疗AD,能有效改善患者的认知功能和日常生活能力,延缓大脑功能衰退,安全性高,且疗效优于单用多奈哌齐。  相似文献   

17.
认知功能损害患者睡眠障碍患病率高,表现形式多样,主要包括:失眠、日间过度思睡、睡眠呼吸障碍、异态睡、不宁腿综合征、睡眠节律紊乱等。阿尔茨海默病(Alzheimer"s disease,AD)是最常见的认知损害类型,73%的中国汉族AD患者伴有睡眠障碍,其中53%伴有不同程度的睡眠节律紊乱。AD患者睡眠障碍在病程中后期较为突出,所以一直以来睡眠节律紊乱都被认为是AD相关神经退行性变的结果,例如“日落现象”,患者一到傍晚就焦虑不安、难以入睡,而白天则睡眠过多。但近期研究表明,睡眠节律紊乱很可能参与AD发生的始动环节。国外前瞻性的随访研究发现,睡眠节律紊乱的认知正常老年人群,在5-10年后更容易发生AD。目前,关于睡眠节律紊乱究竟通过何种途径促使神经系统退行性变发生的研究尚不深入,本文将回顾睡眠节律紊乱引发AD相关病理、生物标记物变化的研究报道。  相似文献   

18.
目的:运用中药辨证治疗与传统认知训练,联合虚拟现实情景互动技术,对轻度阿尔兹海默病患者进行早期认知干预,观察其疗效。方法:将符合纳入条件的68例患者,随机分为对照组(n=34例)和治疗组(n=34例),均予每周6天、连续6个月的治疗,对照组给予中药辨证论治结合传统认知训练,治疗组在对照组的基础上联合虚拟现实情景互动(Anokan-VR)技术治疗。采用简易智能精神状态检查量表(MMSE),功能独立性评定(FIM)量表、韦氏记忆测验修订版(WMS,1999)对两组患者治疗前及治疗后的疗效进行评价比较。结果:治疗前后两组的MMSE评分、FIM评分、WMS评分,均有显著性变化(P0.05);且治疗后治疗组的效果明显优于对照组(P0.05或P0.01)。结论:传统认知训练结合中药辨证论治,可改善轻度阿尔兹海默病患者的认知功能,在此基础上联合虚拟现实情景互动技术,疗效更佳。  相似文献   

19.
目的:探讨血尿酸(UA)水平与初诊帕金森病(PD)患者轻度认知功能障碍的相关性。方法:选取在我 院第一次就诊并未进行任何抗PD治疗的80 例PD患者为PD组,随机选取同期我院体检的70 例体检者为对 照组。测定所有个体晨空腹血UA及肌酐(SCr)浓度;根据Hoehn-Yahr 分级(H-Y 分级)及帕金森病轻度认 知功能障碍(PD-MCI)诊断标准将PD组分为不同亚组。结果:2 组的血UA、蒙特利尔认知评估量表(Mo- CA)值比较差异有统计学意义(P<0.05)。PD-MCI亚组、PD-NCI 亚组的UA浓度低于对照组,PD-MCI亚组 的UA浓度低于PD-NCI亚组(均P<0.05)。对于男性或女性个体,PD-MCI亚组、PD-NCI亚组的UA浓度低于 对照组,PD-MCI亚组的UA浓度低于PD-NCI亚组(均P<0.05)。PD-MCI组中,PD早期亚组、中期亚组的Mo- CA值低于对照组,PD早期亚组MoCA值高于中期亚组(均P<0.05);PD早期亚组、中期亚组UA浓度低于对照 组(均P<0.05)。UA浓度与PD患者MoCA量表的命名能力具有正相关性,与其余认知领域无明显相关性。 结论:血UA浓度的降低可能是PD的发生及其认知功能下降的机制之一。  相似文献   

20.
《Annals of medicine》2013,45(5):437-440
The genetic data, implicating mutations framing the beta-amyloid segment of the amyloid precursor protein as causes of Alzheimer's disease are reviewed and integrated with information on the normal processing of the amyloid precursor protein. The data indicating that there is a second and quantitatively major locus for early-onset Alzheimer's disease on the long arm of chromosome 14 are reviewed. The prediction that this second genetic locus will produce a protein intimately involved in the metabolism of the amyloid precursor protein is reiterated, together with the prediction that all causes of Alzheimer's disease will directly involve this process.  相似文献   

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