血浆hs-CRP和Hcy水平与血管性痴呆患者认知功能的关系

目的:探讨血浆超敏C反应蛋白(hs-CRP)和同型半胱氨酸(Hcy)水平与血管性痴呆(VD)患者认知功能的相关性。方法:回顾性分析2011年12月-2014年7月间我院100例脑梗死住院患者的临床资料,按诊断结果,将患者分为VD组55例和非VD组45例,另选取同期50例健康体检者为对照组。检测并比较3组血浆hs-CRP和Hcy水平,采用简易精神状态速检表(MMSE)对VD组进行痴呆程度分类,分析其与血浆hs-CRP和Hcy的相关性。结果:血浆Hcy与hs-CRP在3组间差异有统计学意义(P0.05),且VD组、非VD组均显著高于对照组,VD组显著高于非VD组,差异均有统计学意义(P0.05)。随着痴呆程度的加重,MMSE评分逐渐降低,血浆hs-CRP与Hcy水平则逐渐升高,差异有统计学意义(P0.05)。经相关性分析发现,MMSE评分和血浆hs-CRP与Hcy水平均呈负相关(r=-0.672,-0.703,P0.05)。结论:血浆hs-CRP与Hcy水平与VD患者的认知功能负相关,临床加强对两指标的检测对VD的诊断及防治有着重要的临床意义。     

血浆同型半胱氨酸与帕金森病临床关系的研究

目的:探讨帕金森病(PD)患者血浆同型半胱氨酸(Hcy)的变化及其与PD严重程度、运动、认知及抑郁之间的相关性。方法:比较53例PD患者及正常对照组血浆Hcy及维生素B12、叶酸水平。并对血浆Hcy与叶酸及维生素B12水平进行相关性分析。采用统一的Hoehn and Yahr(修正)分期量表(HY)、PD评价量表(UPDRS)运动分量表(UPDRS III)、简易智能精神量表(MMSE)、汉密尔顿抑郁量表(HMDS)对PD患者进行评分,分析Hcy与PD患者严重程度、运动、认知功能及抑郁的相关性。结果:PD组及对照组的Hcy浓度分别是(16.2±3.1)、(10.1±2.6)μmol/L,PD组血浆Hcy明显高于对照组,差异有统计学意义(P0.05)。相关分析示被检者血浆Hcy水平与叶酸及维生素B12水平存在负相关。PD患者Hcy水平与HY、UPDRSIII、MMSE、HMDS评分具有显著性相关(分别为r=0.483,r=0.525,r=-0.429,r=0.481,P均0.05)。结论:PD患者血浆Hcy水平升高,与维生素B12、叶酸呈负相关。PD患者Hcy水平和疾病严重程度、运动、认知程度、抑郁倾向相关。     

血浆同型半胱氨酸水平与轻度认知功能障碍的相关性分析

目的:探讨轻度认知功能障碍(MCI)与血浆同型半胱氨酸(Hcy)水平的关系。方法:测定96例MCI及85例健康体检者得血浆Hcy、叶酸及维生素B12水平;MCI患者中选择高Hcy血症者62例,按照是否接受叶酸、维生素B12治疗随机分为治疗组和非治疗组,观察治疗前后Hcy水平及MMSE评分变化。结果:MCI组血浆Hcy水平显著高于对照组(P<0.05),叶酸、维生素B12及MMSE评分低于对照组(P<0.05);MCI组中Hcy水平与叶酸、维生素B12及MMSE评分均呈负相关(P<0.05);治疗后治疗组Hcy水平较治疗前显著下降(P<0.05);治疗组Hcy低于非治疗组(P<0.05);治疗组MMSE评分较治疗前升高,但无显著性差异(P>0.05),治疗组MMSE评分与非治疗组相比差异无统计学意义(P>0.05)。结论:血浆Hcy升高是MCI的重要因素,补充叶酸、维生素B12可降低血浆Hcy水平。     

血清BDNF、IGF-1及Hcy与癫痫患者认知功能损害关系研究

为探讨血清脑源性神经营养因子(BDNF)、胰岛素样生长因子-1 (IGF-1)及同型半胱氨酸(Hcy)与癫痫患者认知功能损害(MCI)的关系,本研究选取2015年1月至2016年10月由本院收治并确诊的癫痫患者116例,根据患者是否发生轻度认知障碍(MCI),将患者分为MCI组50例、非MCI组66例,选取健康体检对象60例作为对照组,检测各组血清BDNF、IGF-1、Hcy水平,并采用韦氏成人智力量表中国修订本(WAIS-RC)对三组患者进行测量,并分析血清BDNF、IGF-1、Hcy与WAIS-RC量表评分的关系。结果显示,与非MCI组和对照组比较,MCI组患者的血清Hcy水平明显升高(p0.05),MCI组患者的血清BDNF、IGF-1水平明显降低(p0.05);非MCI组患者的血清Hcy水平明显高于对照组(p0.05),非MCI组患者的血清BDNF、IGF-1水平明显低于对照组(p0.05);MCI组患者的VIQ、PIQ、FIQ量表评分明显低于非MCI组和对照组(p0.05);非MCI组患者的VIQ、PIQ、FIQ量表评分与对照组比较,差异无统计学意义(p0.05);MCI组患者的VIQ、PIQ、FIQ量表评分与血清BDNF、IGF-1水平呈显著的正相关关系(p0.05);MCI组患者的VIQ、PIQ、FIQ量表评分与血清Hcy水平呈显著的负相关关系(p0.05)。本研究发现癫痫患者MCI血清BDNF、IGF-1水平显著降低、Hcy显著升高,说明血清BDNF、IGF-1和Hcy水平与患者MCI程度有一定的相关性。     

老年痴呆患者脂糖代谢指标及血清CRP、IL-6和TNF-α的表达及临床意义

目的:检测老年痴呆患者体内的脂糖代谢指标及C反应蛋白(CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)的表达水平,并分析其临床意义。方法:选取2014年2月至2016年4月成都市第五人民医院神经内科收治的61例老年痴呆患者,其中阿尔茨海默病(AD)患者32例(AD组)、血管性痴呆(VD)患者29例(VD组),另选取30例健康体检者作为对照组,对比三组受试者的脂糖代谢指标胰岛素降解酶(IDE)、空腹胰岛素(FINS)、空腹血糖(FPG)、胰岛素抵抗指数(HOMA-IR)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)及炎症因子CRP、IL-6、TNF-α的水平,统计并比较各组基础疾病情况。结果:AD组及VD组的FPG、TC、TG及LDL-C水平均高于对照组,而IDE、HDL-C低于对照组,差异均具有统计学意义(P0.05);AD组及VD组患者血清CRP、IL-6、TNF-α水平均高于对照组,且VD组高于AD组,差异均具有统计学意义(P0.05);VD组高血压、糖尿病、冠心病发病率明显高于AD组和对照组(P0.05),AD组和VD组高血脂发病率比较差异无统计学意义(P0.05),但与对照组比较明显升高(P0.05)。结论:糖脂代谢异常及CRP、IL-6、TNF-α均参与AD与VD的发生发展过程,调节血糖、血脂及进行抗炎治疗有助于对老年痴呆患者进行早期干预和治疗。     

针灸联合十八段锦治疗对中风偏瘫患者运动功能影响

目的:研究针灸联合十八段锦治疗对中风偏瘫患者运动功能的影响。方法:选择2017年1月~2019年12月我院中医科针灸门诊针灸治疗的201例中风偏瘫患者,随机分为两组。对照组采用常规治疗,观察组采用针灸联合十八段锦治疗。治疗前后,比较两组的血清基质金属蛋白酶-9 (Matrix metalloproteinases-9,MMP-9)、促红细胞生成素(Erythropoietin,EPO)、同型半胱氨酸(Homocysteine,Hcy)水平、Tinetti步态评估量表(Tinetti gait assessment,TGA)以及功能性步行量表(functional ambulation category,FAC)评分。结果:观察组中风偏瘫患者的有效率明显高于对照组(P<0.05);治疗后,两组的血清MMP-9、EPO、Hcy水平均明显降低(P<0.05),FAC分级和TGA评分均明显升高(P<0.05),且观察组上述指标低于对照组(P<0.05)。结论:针灸联合十八段锦治疗能明显改善中风偏瘫患者的运动功能,提高疗效,其机制可能与降低血清MMP-9、EPO、Hcy水平有关,值得进行推广。     

奥卡西平与丙戊酸钠对癫痫患者血液学指标、认识功能及生活质量的影响

目的:探讨奥卡西平与丙戊酸钠对癫痫患者血液学指标、认识功能及生活质量的影响。方法:将2015年6月至2017年5月我院接诊的癫痫患者98例纳入本研究,随机分为观察组(n=49)和对照组(n=49),对照组给予丙戊酸钠治疗。观察组给予奥卡西平治疗。比较两组同型半胱氨酸(Hcy)、不对称二甲基精氨酸(ADMA)水平、简明精神状态检查量表(MMSE)评分、癫痫患者生活质量量表(QOLIE)评分,并比较两组不良反应发生情况。结果:治疗后两组患者Hcy、ADMA水平均高于治疗前,差异有统计学意义(P0.05),但治疗前和治疗后两组患者Hcy、ADMA水平组间比较差异均无统计学意义(P0.05)。观察组治疗后MMSE评分高于治疗前和对照组(P0.05);对照组治疗前后MMSE评分对比,差异无统计学意义(P0.05)。两组患者治疗后QOLIE各项评分高于治疗前(P0.05),观察组治疗后精力/疲乏、认知功能、药物影响等评分以及总评分高于对照组(P0.05)。观察组不良反应发生率为4.08%,与对照组的10.20%比较差异无统计学意义(P0.05)。结论:奥卡西平与丙戊酸钠治疗癫痫患者均可升高其Hcy、ADMA水平,无严重不良反应发生,而奥卡西平在改善癫痫患者的认知功能和生活质量等方面优于丙戊酸钠。     

阿尔茨海默病患者血清P-tau-181、8-OHdG、Lp-PLA2水平与认知功能的关系及其预测价值分析

摘要 目的：探讨阿尔茨海默病（AD）患者血清磷酸化Tau蛋白-181（P-tau-181）、8-羟基脱氧鸟苷酸（8-OHdG）、脂蛋白相关磷脂酶A2（Lp-PLA2）水平与认知功能的关系及其预测价值。方法：选择2018年1月～2019年12月我院收治的AD患者90例作为AD组,血管源性痴呆（VD）患者90例作为VD组,同期于我院进行体检的健康者90例作为对照组,比较各组血清P-tau-181、8-OHdG、Lp-PLA2水平、蒙特利尔认知评估量表（MoCA）、简易智力状态检查量表（MMSE）、临床痴呆评定量表（CDR）评分,比较不同认知功能障碍程度AD患者血清P-tau-181、8-OHdG、Lp-PLA2水平,并分析各指标的相关性,应用ROC曲线分析血清P-tau-181、8-OHdG、Lp-PLA2水平对AD的预测价值。结果：AD组血清P-tau-181、8-OHdG、Lp-PLA2水平显著高于VD组和对照组（P＜0.05）,VD组和对照组血清P-tau-181、8-OHdG、Lp-PLA2水平比较无统计学差异（P>0.05）。AD组、VD组MoCA、MMSE评分显著低于对照组,CDR评分显著高于对照组（P＜0.05）,AD组和VD组MoCA、MMSE和CDR评分比较无统计学差异（P>0.05）。随着AD患者认知功能的降低,患者血清P-tau-181、8-OHdG、Lp-PLA2水平逐渐升高（P＜0.05）。Pearson相关性分析显示,AD患者血清P-tau-181、8-OHdG、Lp-PLA2与MoCA、MMSE评分呈负相关,与CDR评分呈正相关（P＜0.05）。ROC曲线分析显示,P-tau-181、8-OHdG、Lp-PLA2诊断AD的敏感度分别为88.55%、89.34%、89.77%,特异度分别为81.94%、82.56%、85.67%。结论：AD患者血清P-tau-181、8-OHdG、Lp-PLA2水平异常升高,其水平可以反映患者认知功能障碍程度,对AD的早期诊断和防治具有一定价值。     

高压氧联合叶酸治疗老年脑小血管病患者认知功能及血浆Hcy变化研究

摘要 目的：研究高压氧联合叶酸治疗老年脑小血管病患者认知功能及血浆Hcy变化。方法：选取2019年1月~2020年6月我院收治的80例老年脑小血管病患者作为研究对象,随机将其分为两组,对照组50例,给予叶酸治疗,研究组30例,给予高压氧联合叶酸治疗,观察两组患者治疗后的疗效、认知功能、血浆Hcy水平、生活质量及不良反应。结果：治疗前,两组的蒙特利尔认知评估量表(Montreal Cognitive Assessment,MoCA)认知功能评分、血浆Hcy水平、日常生活能力量表(Activity of Daily Living Scale,ADL)评分对比无差异（P>0.05）,治疗后两组的MoCA认知功能评分、ADL评分均升高,血浆Hcy水平均降低,且观察组变化优于对照组( P<0.05);治疗期间对照组不良反应发生情况为13.33 %,观察组不良反应发生情况为16.00 %,两组对比差异无统计学意义（P>0.05）;研究组总有效率显著高于对照组（93.33 % vs.74.00 %,P<0.05）。结论：高压氧联合叶酸治疗老年脑小血管病患者疗效显著,能显著改善患者的认知功能和Hcy水平,提高其日常生活能力,且安全性高,值得临床应用。     

美金刚联合普拉克索治疗帕金森患者临床疗效及对CysC、Hcy水平影响

目的:探究美金刚联合普拉克索在治疗帕金森患者中的临床疗效,并就治疗对患者胱抑素C(cystatin C,CysC)以及血同型半胱氨酸(homocysteine,Hcy)水平的影响。方法:选择2018年1月至2020年1月于我院接受治疗的98例帕金森患者,随机数字表法均分为两组(每组各49例),对照组单纯接受美金刚治疗,研究组在对照组基础上加用普拉克索进行治疗,对比两组治疗有效率,治疗前后CysC、Hcy水平,以及治疗前后简易智能精神状态检查量表(mini mental state examination,MMSE)以及帕金森病评定量表III(parkinson comprehensive rating scale,UPDRS III)评分,最后对两组患者治疗中不良反应发生率进行统计对比。结果:(1)研究组患者治疗有效率明显高于对照组患者(P0.05);(2)治疗前两组患者CysC、Hcy水平对比差异不具有统计学意义(P0.05),治疗后研究组患者CysC、Hcy水平低于对照组(P0.05);(3)治疗前两组患者MMSE及UPDRS III量表评分对比差异不具有统计学意义(P0.05),治疗后研究组患者MMSE得分高于对照组,UPDRS III量表评分低于对照组(P0.05);(4)两组治疗不良反应诸如胃肠道反应、嗜睡、体位性低血压等对比无差异(P0.05)。结论:美金刚联合普拉克索对帕金森具有较好的治疗效果,能够显著改善患者认知及运动功能,降低CysC、Hcy水平,同时治疗安全性较高。     

Effect of homocysteine and nitric oxide levels on specific Computed Axial Tomography measurements in Alzheimer disease

The present study was undertaken to examine the effect of Homocysteine (Hcy) and nitric oxide (NO) levels on specific Computed Axial Tomography (CAT) measurements, as global brain atrophy and brain vascular lesion in Alzheimer Disease (AD) and in Vascular Dementia (VD) patients. We have analysed serum Hcy and NO levels in AD patients and compared the findings with those in VD patients and control subjects. Moreover we have studied the correlation of Hcy and NO levels with cognitive impairment and brain atrophy determined by Computed Axial Tomography. Hcy serum levels significantly increased in all demented patients compared to control group, independently from the dementia type. On the contrary, no differences were observed in NO serum levels between groups. Moreover, we found significant correlation between Hcy and brain atrophy in both demented groups; whereas NO levels correlated only in AD, but not in VD patients. The pathogenic effect of Hcy either in AD and VD patients appears to confirm a definitive vascular component in AD. As regards NO, our results highlight the role of NO as a beneficial molecule in AD and support the use of NO mimetics as an antineurodegenerative therapy for AD patients.     

Polymorphism of Apolipoproteine E in Relation with Alzheimer and Vascular Dementia

Summary 1. The epsilon 4 allele of the apolipoprotein E gene increases the risk of late onset familial and sporadic Alzheimer disease. Relation of epsilon 4 allele of the apolipoprotein E gene to various types of dementia and the onset of dementia were analyzed in the present study.2. The study comprised 139 patients (50 men and 89 women) with dementia, mean age 73.61 years (range 47–98). The diagnosis of dementia was made according to Diagnostic and Statistical Manual of Mental Disorders, and subtypes diagnoses were made according to NINCDS-ADRDA and NINDS-AIREN criteria. Minimental State Examination (MMSE) was used for the screening of dementia. Apolipoprotein E polymorphism was determined by the PCR-RFLP technique-polymerase chain reaction and subsequent digestion with specific restriction endonuclease. For statistical analyses chi-square test and the crude Gart′s odds ratio (OR) and 95% confidence intervals (CI) were used.3. From 139 dementia patients (MMSE ≤24 points) in 61 (45%) Alzheimer disease (AD) was present, in 44 patients (31%) vascular dementia (VD), and in 34 (24%) mixed dementia (MD) were revealed. In comparison with control group the presence of at least one ApoE-ɛ4 allele was significantly higher only in the group with AD (p < 0.001), (OR=2.76; 95%: 1.42–5.36). The frequency of ɛ4 allele carriers was significantly overrepresented in AD group compared with VD (χ²=5.94; p=0.0148). Differences between AD and MD or VD and MD were not confirmed.     

Spatial analysis of the neuronal density of aminergic brainstem nuclei in primary neurodegenerative and vascular dementia: a comparative immunocytochemical and quantitative study using a graph method.

A graph method was employed to analyse spatial neuronal patterns of pontine nuclei with ascending aminergic projections to the forebrain (nucleus centralis superior (NCS), raphes dorsalis (NRD) and locus coeruleus (LC)), in Alzheimer disease (AD), Huntington disease (HD), and vascular (VD) as well as "mixed-type" (VA) dementia, compared with non-demented controls (CO) and a small sample of brains from schizophrenics ("dementia praecox" (DP)). The quantitative evaluations by the "minimal spanning tree (MST)" were complemented by rough neurofibrillary tangle (NFT) counts and by semiquantitative immunohistochemical assessment of amyloid deposition, neuritic plaque formation, and cellular gliosis. The AD cases showed a significant decline of neuronal density in all nuclei examined, as compared with controls and DP. Neuronal loss was not significant in VD, while the mixed cases with both vascular and Alzheimer-type pathology exhibited pronounced changes of neuronal density. Amyloid deposition occurred almost exclusively in AD and VA, as a rule, being of moderate degree, except for two presenile AD cases where it was marked. NFT were significantly increased in all nuclei in AD and in the VA cases, while they only occasionally appeared beyond age 55 in HD, DP and CO. The four HD cases showed in the NCS and NRD neuronal loss as severe as in AD. This neuronal loss implicates impairment of serotoninergic and noradrenergic neuromodulation as one basic mechanism promoting dementia in AD, VA and perhaps in HD.     

Lipid Peroxidation and Antioxidant Enzyme Activities in Vascular and Alzheimer Dementias

It has been reported that oxidative stress may play a role in the pathogenesis of dementia of the Alzheimer type (AD) and the cerebral ischemia which causes vascular dementia (VD). We measured malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) activities in blood samples from patients with AD and VD and in healthy non-demented controls (CTR) which similar ages to the patients, in order to evaluate the degree of oxidative stress in patients with AD and VD. A sample of 150 subjects consisting of 50 patients with AD; 50 patients with VD and 50 CTR, aged from 65 to 85 years on, was analyzed. Most of the changes observed were in SOD activity and MDA levels. Catalase activity were least affected. Significant differences were observed in SOD and GR activity between males and females in CRT and in patients with AD, but not in VD. We have found a decrease in antioxidant enzymes activities (SOD, CAT, GPx and GR) in patients with AD and VD and significant differences were observed between CRT and AD patients for ages from 65 to 74, 75 to 84 and from 85 years to 94 years in SOD activity and MDA levels (P < 0.001). MDA levels increase with age in VD, AD and CTR. No significant variation with respect to sex were detected, but significant variations in MDA levels were detected between CRT and patients with VD and AD (P < 0.001). We conclude that oxidative stress plays an important role in the brain damage for both AD and VD, being observed higher levels of oxidative stress for AD that for VD.     

Evaluation of Selenium,Redox Status and Their Association with Plasma Amyloid/Tau in Alzheimer’s Disease

The aim of the study was to evaluate blood selenium and antioxidants as possible oxidative stress markers in Alzheimer’s disease (AD) along with amyloid β42 (Aβ42) and tau by comparing them with vascular dementia (VD) and age-matched healthy controls. Selenium, total tau, Aβ42, glutathione (GSH) and malondialdehyde (MDA) levels and the activities of antioxidant enzymes were analysed in the blood of AD patients (n?=?30), VD patients (n?=?35) and controls (n?=?40) from South India. Plasma Aβ42 level was significantly higher (P?<?0.001) in both AD and VD compared to controls. Total tau and tau-to-amyloid ratio were significantly lower in both AD and VD (P?<?0.001), compared to controls, and a significant difference (P?<?0.01 and P?<?0.05, respectively) was also observed between AD and VD. The receiver operating characteristic (ROC) curve-derived cutoff values of <3.5 for tau-to-Aβ42 ratio and <520 pg/ml for total tau showed sensitivity and specificity of around 67–72 % for differentiating AD from VD and around 90 % for AD from controls, indicating that they could serve as reliable AD-specific markers. The MDA levels were significantly higher (P?<?0.001) in both dementia groups along with a significant decrease (P?<?0.001) in reduced GSH levels, indicating elevated oxidative stress and altered redox status in both forms of dementia. Selenium levels did not vary significantly between the three groups. The activity of glutathione peroxidase increased in both AD and VD compared to controls, with a concomitant decrease in glutathione reductase and glucose-6-phospate dehydrogenase (P?<?0.001) activity. The activity of thioredoxin reductase was significantly lower in both patient groups (P?<?0.001) compared to healthy controls. No correlation was observed between selenium and activities of selenoenzymes, tau, Aβ42 or tau-to-Aβ42 ratio, when analysing independently, indicating that blood selenium may not be directly involved in Aβ production and in regulating tau/Aβ42-mediated mechanism in AD. The present study emphasizes the enhanced oxidative stress in AD pathology and plasma tau and tau-to-amyloid ratio as possible markers to differentiate AD from VD. The study also points that blood selenium may not be involved in regulating oxidative stress in AD, and a longitudinal study correlating plasma and cerebrospinal fluid (CSF) selenium and selenoprotein levels is warranted.     

血清NGF、BDNF、GFAP水平与老年血管性痴呆严重程度的相关性分析

目的:探讨血清神经生长因子(Nerve Growth Factor,NGF)、脑源性神经营养因子(Brain Derived Neural Nutrition Factor, BDNF)、胶质纤维酸性蛋白(Glial Fibrillary Acidic Protein,GFAP)水平与老年血管性痴呆严重程度的相关性。方法:选择我院2016年1月至2018年12月收治的81例老年血管性痴呆患者,根据简易精神状态检查表(MMES)评分将其分为三组,以MMSE评分21～26分者为轻度组(26例),10～20分者为中度组(28例),0～9分者为重度组(27例),同时选择来院体检的50例健康者作为对照组,检测和比较各组的血清NGF、BDNF、GFAP水平,分析血清NGF、BDNF、GFAP水平与老年血管性痴呆患者MMSE分值的相关性。结果:老年血管性痴呆者的血清NGF、GFAP水平明显高于对照组(P0.05),血清BDNF水平明显低于对照组(P0.05)。轻度组、中度组、重度组的血清NGF、GFAP、BDNF水平对比差异均有统计学意义(P0.05):NGF水平:轻度组中度组重度组,BDNF水平:轻度组中度组重度组;GFAP水平:轻度组中度组重度组。血清NGF、BDNF水平与MMSE分值评分呈显著正相关(r_1=0.652,r_2=0.671,P0.05),血清GFAP水平与MMSE分值呈显著负相关(r3=-0.681,P0.05)。结论:血清NGF、BDNF、GFAP水平均与老年血管性痴呆的严重程度密切相关,可能用于评估老年血管性痴呆病情的严重程度。     

Plasma 24S-hydroxycholesterol (cerebrosterol) is increased in Alzheimer and vascular demented patients

Alzheimer's disease (AD) is characterized by the presence of senile plaques, neurofibrillary tangles, and neuronal cell loss associated with membrane cholesterol release. 24S-hydroxycholesterol (24S-OH-Chol) is an enzymatically oxidized product of cholesterol mainly synthesized in the brain. We tested the hypothesis that plasma levels of this oxysterol could be used as a putative biochemical marker for an altered cholesterol homeostasis in the brain of AD patients. Thirty patients with clinical criteria for AD, 30 healthy volunteers, 18 depressed patients, and 12 patients with vascular dementia (non-Alzheimer demented) were studied. Plasma concentrations of 24S-OH-Chol were assayed by isotope dilution;-mass spectrometry, cholesterol was measured enzymatically, and apolipoprotein E (apoE) was genotyped by polymerase chain reaction and restricted fragment length polymorphism. The concentration of 24S-OH-Chol in AD and non-Alzheimer demented patients was modestly but significantly higher than in healthy controls and in depressed patients. There was no significant difference in the concentrations of 24S-OH-Chol between depressed patients and healthy controls nor between AD and non-Alzheimer demented patients. The apoE straightepsilon4 allele influences plasma 24S-OH-Chol. However, this influence could be completely accounted for by the elevated plasma cholesterol in apoE4 hetero- or homozygotes. Plasma 24S-OH-Chol levels correlated negatively with the severity of dementia. AD and vascular demented patients appear to have higher circulating levels of 24S-OH-Chol than depressed patients and healthy controls. We speculate that 24S-OH-Chol plasma levels may potentially be used as an early biochemical marker for an altered cholesterol homeostasis in the central nervous system. 24S-hydroxycholesterol (cerebrosterol) is increased in Alzheimer and vascular demented patients.     

The Science of Vascular Contributions to Cognitive Impairment and Dementia (VCID): A Framework for Advancing Research Priorities in the Cerebrovascular Biology of Cognitive Decline

The World Health Organization reports that 47.5 million people are affected by dementia worldwide. With aging populations and 7.7 million new cases each year, the burden of illness due to dementia approaches crisis proportions. Despite significant advances in our understanding of the biology of Alzheimer’s disease (AD), the leading dementia diagnosis, the actual causes of dementia in affected individuals are unknown except for rare fully penetrant genetic forms. Evidence from epidemiology and pathology studies indicates that damage to the vascular system is associated with an increased risk of many types of dementia. Both Alzheimer’s pathology and cerebrovascular disease increase with age. How AD affects small blood vessel function and how vascular dysfunction contributes to the molecular pathology of Alzheimer’s are areas of intense research. The science of vascular contributions to cognitive impairment and dementia (VCID) integrates diverse aspects of biology and incorporates the roles of multiple cell types that support the function of neural tissue. Because of the proven ability to prevent and treat cardiovascular disease and hypertension with population benefits for heart and stroke outcomes, it is proposed that understanding and targeting the biological mechanisms of VCID can have a similarly positive impact on public health.     

静止性脑梗死与血管性痴呆相关性的病例对照分析

目的　探讨静止性脑梗死 (SCI)与血管性痴呆 (VD)的关系。　方法　采用病例对照的方法对 1 2 6例血管性痴呆病人和 1 2 6例非痴呆病人进行 CT或 MRI检查 ,比较两组 SCI的发生状况。　结果　1 2 6例 VD中发现 SCI5 3例 (4 2 .1 % ) ,1 2 6例非痴呆病人中发现 SCI2 2例 (1 7.5 % ) ,两组比较有高度显著性差异 (P <0 .0 1 )。　结论　 SCI与 VD密切相关