高同型半胱氨酸血症与糖尿病合并血管性痴呆的相关性分析

目的探讨高同型半胱氨酸血症与糖尿病合并血管性痴呆的相关性。方法选取糖尿病合并血管性痴呆患者、非痴呆性血管性认知功能障碍患者、单纯糖尿病患者各60例,分别设为痴呆组、认知障碍组、对照组,采用简易精神状态量表与蒙特利尔认知评估量表进行评估,比较其认知功能评分。采血测定血浆同型半胱氨酸水平,比较3组同型半胱氨酸水平、高同型半胱氨酸血症发生率。根据高同型半胱氨酸血症发生情况将每组分为A组(高同型半胱氨酸血症)、B组(非高同型半胱氨酸血症),比较其认知功能评分。结果 3组MMSE评分、MoCA评分比较差异均有统计学意义(P0.05)。3组同型半胱氨酸水平、高同型半胱氨酸血症发生率比较差异均有统计学意义(P0.05)。痴呆组、认知障碍组、对照组中,A组MMSE评分、MoCA评分均低于B组(P0.05)。高同型半胱氨酸血症与糖尿病合并血管性痴呆呈正相关(r=0.809,P0.05)。结论高同型半胱氨酸血症与糖尿病合并血管性痴呆密切相关,同型半胱氨酸水平越高,认知功能损害越严重。     

同型半胱氨酸与阿尔茨海默病及血管性痴呆

目的研究同型半胱氨酸(Homocysteine,Hcy)及叶酸、维生素B_(12)与阿尔茨海默病(Alzheimer Dis- ease,AD)和血管性痴呆(Vascular dementia,VaD)的关系,并通过Hcy揭示AD发病的血管危险因素。方法用美国国立神经病学、语言障碍和卒中-阿尔茨海默病和相关疾病学会(NINCDS-ADRDA)标准的可能标准严格筛选AD患者35例,用ADDTC诊断标准筛选VaD患者30例,并同期选择31例无临床脑血管病史、无认知功能障碍的健康查体中心志愿者为对照组。取肝素抗凝的血浆用循环酶法进行Hcy的测定。取血清由全自动化学发光免疫检测仪进行叶酸和维生素B_(12)的测定。结果AD组和VaD组血浆Hcy水平显著高于对照组,血清叶酸和VitB_(12)水平显著低于对照组。VaD组存在痴呆程度越高血浆Hcy水平越高这一显著正相关关系,而AD组这一正相关关系无统计学意义;且发现VaD组患者MMSE评分越低其血浆Hcy水平越高这一显著负相关关系,而AD组这一关系仍无统计学意义。在所有研究对象中存在血浆Hcy水平与血清叶酸及VitB_(12)水平的显著负相关关系。结论提示高Hcy血症可能是引起AD和VaD的一个重要危险因素,Hcy作为一个新的血管因素加强了AD与血管危险因素之间的联系,并且提示积极治疗高Hcy血症在预防AD和VaD方面可能有积极意义。     

痴呆患者心理和行为症状特征以及利培酮疗效的研究

目的　比较痴呆各亚型心理和行为症状 (BPSD)的特征 ,评价利培酮治疗BPSD疗效与安全性 ,探讨血浆同型半胱氨酸(Hcy)水平与BPSD的关系。方法　采用Alzheimer病行为症状评定量表 (BEHAVE AD)、Cohen Masfield激惹性问卷 (CMAI)评定阿尔茨海默病 (AD)、阿尔茨海默病混合型 (MD)、血管性痴呆 (VD)各 3 0例和正常对照组 3 0名的BPSD。 66例痴呆患者应用利培酮 (1 5mg/d)治疗 6周。采用副反应量表 (TESS)评价副反应。采用高压毛细管电泳紫外检测法测定经 2 ,4一二硝基氟苯 (DNFB)衍生后的血浆Hcy水平。结果　AD患者激惹、焦虑与恐惧发生率较高 ,VD患者无目的游荡发生率和严重程度均较低 ,MD患者BPSD症状无特异性。利培酮能明显改善痴呆患者BPSD ,且不损害认知功能 ,副反应主要为轻度嗜睡 ,肌强直 ,震颤。AD、MD和VD患者血浆Hcy浓度均显著高于正常对照组 ,血浆高Hcy水平的痴呆患者BEHAVE AD总分较高。结论　AD、VD患者BPSD症状有特异性 ,MD患者BPSD表现无特异性。利培酮能有效改善痴呆患者BPSD且安全。血浆高Hcy水平在痴患者BPSD的发病机制中可能起重要作用。     

Hhcy对脑小血管病患者认知功能的影响

目的探讨高同型半胱氨酸血症(Hhcy)对脑小血管病(SVD)患者认知功能的影响。方法 142例SVD患者根据认知功能分为痴呆组、认知功能障碍非痴呆组、认知功能正常组,测定研究对象血浆同型半胱氨酸(Hcy)水平及MMSE、画钟测验评分。结果 (1)Hcy水平痴呆组明显高于认知功能障碍非痴呆组(P<0.05),认知功能障碍非痴呆组高于认知功能正常组。(2)Logistic回归分析得出Hcy水平升高是小血管病患者认知功能损害的独立危险因素。(3)Hhcy对MMSE总评分、定向功能、语言功能以及反应视空间功能、动作的计划性和执行功能画钟测验均有独立的危险性,其OR值分别为1.044、1.057、1.040、1.251。结论 Hcy水平升高是脑小血管病认知功能损伤的独立危险因素,对总体认知功能、定向功能、语言功能以及视空间功能、动作的计划性和执行功能有独立影响作用。     

高同型半胱胺酸血症与帕金森病认知功能的相关性研究

目的探究高同型半胱胺酸血症与帕金森病认知功能相关性。方法选取我院收治的130例帕金森病患者作为试验组,同期的健康体检人员110例作为对照组,对影响认知功能的可能危险因素进行Logistic回归分析,并将轻度认知功能障碍患者、痴呆患者及健康人群血清高同型半胱胺酸含量进行对比。结果经Logisitc非条件回归分析可见,年龄、文化程度、吸烟、高血压、糖尿病、高密度脂蛋白、低密度脂蛋白、血清总胆固醇、血浆同型半胱氨酸为认知功能障碍的危险因素。对照组与帕金森非认知障碍组、帕金森认知障碍组的血浆同型半胱氨酸含量相比差异均具有统计学意义(t=3.45,P0.05;t=6.43,P0.05)。帕金森非认知功能障碍组与帕金森认知功能障碍组的血浆同型半胱氨酸含量相比差异具有统计学意义(t=5.23,P0.05)。结论帕金森病认知功能障碍患者同型半胱胺酸含量明显高于无认知功能障碍的帕金森病患者及健康人群,高同型半胱胺酸血症为帕金森病认知功能障碍的危险因素,可作为临床医师可靠的诊断依据。     

脑白质疏松症患者的认知水平与血浆同型半胱氨酸水平和颈部血流动力学的相关性

目的 探讨脑白质疏松症(LA)患者认知功能、血浆同型半胱氨酸(Hcy)水平与颈动脉血流动力学指标的关系.方法 测试LA患者认知损害水平,根据结果分为三组,分别为痴呆组、轻度认知功能障碍组和无认知功能障碍组.根据三组患者的血浆Hcy水平及颈部血管超声血流动力学指标进行相关性分析.结果 痴呆组患者的血浆Hcy水平较轻度认知功能障碍组与无认知功能障碍组增高(P<0.05),双侧颈内动脉阻力指数(RI)、搏动指数(PI)亦较轻度认知功能障碍组与无认知功能障碍组增高(P<0.05).结论LA患者不同水平认知功能与血浆Hcy水平和颈部血管超声变化存在相关性,血浆Hcy水平越高,RI和PI越高,则认知损害越重.     

皮质下动脉硬化性脑病及认知功能障碍与血浆同型半胱氨酸水平的关系

皮质下动脉硬化性脑病(SAE)的确切发病机制尚不明了.研究[1,2]表明,高同型半胱氨酸(Hcy)血症是脑血管病的独立危险因素.本研究通过对SAE患者血浆Hcy水平的检测,探讨SAE及认知功能障碍与血浆Hcy水平之间的关系.     

脑梗死患者轻度认知功能障碍与同型半胱氨酸的关系

目的探讨脑梗死患者轻度认知功能障碍与血清中同型半胱氨酸(Hcy)的关系,为预防痴呆提供依据。方法依据简易智能精神状态量表(MMSE),将我院收治的230例脑梗死患者分为2组:轻度认知功能障碍患者86例(MCI组)和认知功能正常患者144例(对照组)。取患者外周空腹血,测定血浆Hcy的水平,进行组间比较。应用非条件Logistic回归分析法分析血浆Hcy水平与MoCA总评分及其各项认知功能以及病灶部位的关系。结果 (1)MCI组测得的血浆Hcy水平均比对照组明显高,差异有统计学意义(P<0.05)。(2)血浆Hcy水平对MoCA总评分、视空间与执行功能、语言功能、基底节病灶、额部病灶、颞部病灶有独立的危险性。结论脑梗死后轻度认知功能障碍(MCI)与血浆Hcy水平呈正相关。     

阿尔茨海默病与脑白质疏松血浆同型半胱氨酸水平的相关性研究

目的探讨阿尔茨海默病(AD)与缺血性脑白质疏松症(LA)、血浆同型半胱氨酸(Hcy)及叶酸、维生素B_(12)水平的相关性。方法采用简易智能状态量表(mini-mental state examation,MMSE)检查患者的认知功能,根据MMSE评分和AD的诊断标准收集病例,共收集AD患者60例,正常对照组64例。通过头颅MRI检查筛选LA病例,AD伴LA者36例,无LA的AD患者24例;对照组无LA 40例,伴LA的正常对照组24例;用化学免疫发光法测定2组血浆同型半胱氨酸、叶酸、维生素B_(12)水平,同时检测所有受试者的血压、血糖、血脂、体重指数、教育情况等。结果与对照组比较,AD组血浆同型半胱氨酸升高(P0.05),叶酸和维生素B_(12)水平下降(P0.05);通过应用R×C资料的卡方检验得出AD组与对照组脑白质疏松发生率差异有统计学意义(P=0.010);对AD组脑白质疏松和认知障碍程度进行Spearman相关性分析得出,AD组认知障碍程度与脑白质疏松程度呈正相关(r_s=0.430,P=0.010)。结论高Hcy可能参与AD的发病,而LA发生加重了认知功能损伤,适当补充叶酸和维生素B_(12)可有助于改善痴呆患者的临床症状。     

高同型半胱氨酸血症与老年人脑梗死的相关性

目的 研究血浆同型半胱氨酸血症(Hcy)与老年人脑梗死的关系.方法 采用循环酶法同型半胱氨酸试剂盒测定50例老年脑梗死患者和40例健康者血浆Hcy水平.结果 病例组与对照组的血浆Hcy水平有显著差异,病例组高于对照组.结论 高同型半胱氨酸血症与老年人脑梗死的危险性增加有关.     

Plasma homocysteine levels and Parkinson disease: disease progression, carotid intima-media thickness and neuropsychiatric complications

OBJECTIVE: To determine whether plasma homocysteine (Hcy) levels are associated with clinical characteristics, neuropsychological and psychiatric manifestations and cardiovascular comorbidity in patients with Parkinson disease (PD). BACKGROUND: Elevated Hcy levels are linked to atherosclerosis, vascular disease, depression, and dementia. Patients with PD treated with L-dopa have been shown to have elevated Hcy levels. DESIGN/METHODS: Idiopathic PD patients were evaluated using the Unified Parkinson's Disease Rating Scale, Hoehn and Yahr stage, Parkinson Psychosis Rating Scale, Beck Depression Inventory, Frontal Assessment Battery, Mini-Mental Status Examination, and several tests for frontal type cognitive functions. Fasting blood samples were collected for the measurement of Hcy, and carotid B-mode ultrasound was performed to measure intima-media thickness of the common carotid arteries. RESULTS: Seventy-two consecutive PD patients (46 men; average age, 68.7 +/- 11.6 years; average disease duration, 7.0 +/- 4.7 years) were recruited. All but 10 patients were treated with L-dopa. The average level of Hcy was 16.4 +/- 7.8 micromol/L, and 38.9% of the patients had Hcy level above the reference range (>15.0 micromol/L). The Hcy levels were associated with PD duration as they were with L-dopa treatment duration but were not associated with the parameters of disease severity or with L-dopa dose. The Hcy levels were associated neither with the common carotid intima-media thickness nor with cardiovascular morbidity. No association was found between Hcy and the neuropsychiatric features of PD such as depression, cognitive performance, or psychosis. CONCLUSIONS: Hyperhomocystinemia is common in L-dopa-treatedPD patients but was not associated with neuropsychological complications (depression, dementia, and cognitive decline associated with frontal lobe functioning or psychosis), enhanced disease severity, or vascular comorbidity.     

The relation between homocysteine levels and development of Alzheimer's disease in mild cognitive impairment patients

The aim of this study was to investigate over a 3-year period the connection between homocysteine (Hcy) levels and development of Alzheimer's disease (AD) in patients with mild cognitive impairment (MCI). Hcy was analyzed in 68 men, mean age 65 years, and 68 women, mean age 64 years. Age, sex, cobalamin, folate, creatinine, and thyroid profiles as well as results of Mini-Mental State Examination at the first visit to the memory investigation unit of a geriatric department were recorded from patient journals collected between 1992 and 1999. The total numbers of persons who converted to AD within a period of 3 years from initial investigation with baseline Hcy sampling was 12 of 46 (26%) males, and 18 of 50 women (36%). The total percentage of men and women converting to AD was 31%. Thirty-three percent of men with Hcy levels >20 micromol/l converted to AD. The corresponding figure for men with Hcy levels 20-17 micromol/l was 50%, whereas none of the 18 men with Hcy levels <17 micromol/l converted to AD. These differences were statistically significant. There was also a statistically significant difference between the percentage of women with Hcy levels >16 micromol/l who converted to AD (45%) as compared to those with Hcy levels <16 micromol/l who converted (21%). These findings are inconsistent with the results of other studies showing a positive correlation with hyperhomocysteinemia and occurrence of AD. However, our findings tentatively suggest a possible protective effect of low/normal Hcy levels on dementia conversion in MCI patients.     

Elevated serum homocysteine level is not associated with serum C-reactive protein in patients with probable Alzheimer’s disease

Elevated plasma homocysteine (Hcy) levels have been associated with Alzheimer’s disease (AD) and cognitive impairment. Studies have shown that Hcy may have direct and indirect neurotoxicity effects. The aim of the study was to investigate serum Hcy concentration in patients with probable AD with age-matched controls and to determine whether there was an association between serum Hcy and C-reactive protein concentration in patients with probable AD. We also aimed to determine whether there was an association between serum tHcy concentration and cognitive impairment in patients with probable AD. Serum concentration of total Hcy was determined by the fluorescence polarization immunoassay on the AxSYM system, and serum C-reactive protein (CRP) concentration was determined by means of particle-enhanced immunonephelometry with the use of BN II analyzer. Cognitive impairment was tested by the MMSE score. Body mass index (BMI) was calculated for each subject included in the study. Age, systolic and diastolic blood pressure and BMI did not differ significantly between the two groups. Mean serum tHcy concentration in the control group of subjects was 12.60 μmol/L, while in patients with probable AD the mean serum tHcy concentration was significantly higher than 16.15 μmol/L (p < 0.01). A significant negative association between serum tHcy concentration and cognitive impairment tested by the MMSE score in patients with probable AD was determined (r = −0.61634; p < 0.001). Positive, although not significant correlation between CRP and serum tHcy concentrations in patients with AD, was observed. Increased tHcy concentration in patients with probable AD, and the established negative correlation between serum tHcy concentration and cognitive damage tested by MMSE score in the same group of patients, suggests the possible independent role of Hcy in the pathogenesis of AD and cognitive impairment associated with this disease.     

Cobalamin, folate, methylmalonic acid, homocysteine, and gastritis markers in dementia

The prevalence of dementia disorders, cobalamin and/or folate deficiency as well as gastritis increases with age. To investigate whether there is an association between these conditions, plasma homocysteine (Hcy), serum methylmalonic acid, serum cobalamin and blood folate concentrations were measured. Gastritis was indirectly diagnosed by measuring serum antibodies against H,K-ATPase, HELICOBACTER PYLORI and intrinsic factor, using enzyme-linked immunosorbent assays. The studied groups consisted of 47 patients with Alzheimer's disease (AD), 9 with AD pathology in combination with additive vascular lesions, 59 with vascular dementia, 8 who were cognitively impaired, and 101 control cases. Plasma Hcy concentrations were significantly elevated in the dementia groups, with the highest levels in patients with vascular pathology. We conclude that hyperhomocysteinemia is a common finding in patients with dementia disorders of different etiologies. The markers for gastritis did not contribute to an elucidation of a possible connection between this condition, dementia disorders, or cobalamin/folate deficiency.     

Gray-matter degeneration in presenile Alzheimer's disease

Previous comparisons between presenile Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT) did not control for disease severity and duration. In the current study, 18 patients with each diagnosis were matched for disease duration, cognitive dysfunction, and behavioral symptoms (using the modified Mini-Mental Status [mMMS] examination and the Blessed Dementia Rating Scale [BDRS] ). Regional cerebral blood flow (rCBF) was quantified by the 133xenon inhalation technique, and several indices of tissue perfusion were examined. The two variables of primary interest were relative gray-matter relative weight (35% in presenile patients versus 39% in senile patients and healthy control subjects, p = 0.006), with neither perfusion nor disease severity differences between the two dementia samples. This loss of gray matter was significantly related to both severity and duration of disease in the patients with presenile AD, but not in patients with SDAT. These findings lend support ot previous suggestions of greater degenerative process in presenile AD and confirm the need to examine and control age of onset in future investigations of AD. Further, correlation analysis suggests greater proportion of common variance among clinical and physiological indices in presenile AD.     

The 894G > T (Glu298Asp) Variant in the Endothelial NOS Gene and MTHFR Polymorphisms Influence Homocysteine Levels in Patients with Cognitive Decline

The presence and severity of cerebrovascular pathological findings have been shown to increase the risk and stage of cognitive decline observed in Alzheimer’s disease and vascular dementia. Thus, the modification of vascular risk factors seems useful to reduce the risk of dementia regardless of type. Hyperhomocysteinemia has long been known as a major independent risk factor for vascular dysfunction. In this study, we evaluated the relationships between plasma homocysteine levels and genetic risk factors for hyperhomocysteinemia, i.e., the presence of gene variants for methylenetetrahydrofolate reductase (MTHFR) and endothelial nitric oxide synthase (eNOS) in patients with cognitive impairment. Genotyping for MTHFR C677T and eNOS 894G > T polymorphisms was carried out in 69 patients with probable diagnosis of AD and anamnestic mild cognitive impairment, matched for age and gender with 69 healthy volunteers. Patients with MTHFR TT677 genotype showed higher plasma Hcy levels than controls, even after adjustment for folate levels (P < 0.05). Moreover, Hcy plasma levels were higher in cases than controls for any given eNOS genotype. In particular, the presence of eNOS TT894 genotype in patients with cognitive decline resulted significantly associated with increased plasma Hcy levels when compared with controls having the same genotype or patients having other eNOS genotypes (P = 0.02). These data suggest that both MTHFR C677T and eNOS G894T variants should be regarded as genetic risk factors for hyperhomocysteinemia in patients with cognitive decline.     

Homocysteine and cognitive impairment in Parkinson's disease: A biochemical,neuroimaging, and genetic study

The role of the plasma level of homocysteine (Hcy), as a primary outcome, and the effect of silent cerebrovascular lesions and genetic variants related to Hcy metabolism, as secondary outcomes, in the cognitive decline and dementia in Parkinson's disease (PD) were studied. This case–control study focused on 89 PD patients of minimum 10 years of evolution and older than 60 years, who were neuropsychologically classified either as cognitively normal (n = 37), having mild cognitive impairment (Petersen criteria) (n = 22), or suffering from dementia (DSM‐IV) (n = 30), compared with cognitively normal age‐matched control subjects (n = 30). Plasma levels of Hcy, vitamins B12 and B6, folic acid, polymorphisms in genes related to Hcy metabolism (MTHFR, MTR, MTRR, and CBS) and silent cerebrovascular events were analyzed. Plasma levels of Hcy were increased in PD patients (P = 0.0001). There were no differences between the groups of patients. The brain vascular burden was similar among PD groups. There was no association between polymorphisms in the studied genes and the Hcy plasma levels or cognitive status in PD patients. We found no evidence for a direct relationship between Hcy plasma levels and cognitive impairment and dementia in PD. No indirect effect through cerebrovascular disease or genetic background was found either. © 2009 Movement Disorder Society