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阿尔茨海默病和血管性痴呆与血糖代谢水平的关系及危险因素分析 被引量:11

Relationship between Alzheimer's Disease, Vascular Dementia and Glucose Metabolism and Their Risk Factors
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摘要 目的:研究阿尔茨海默病和血管性痴呆与血糖代谢水平的关系及危险因素。方法:选取2013年12月到2014年12月我院收治的阿尔茨海默病80例(A组)和血管性痴呆70例(B组),另选取同时期无痴呆者70例(对照组),测量三组入选者血糖各指标水平,并分析阿尔茨海默病和血管性痴呆的危险因素。结果:A组和B组空腹血糖(FPG)均显著高于对照组,胰岛素降解酶(IDE)显著低于对照组,比较差异具有统计学意义(P<0.05);B组糖尿病、冠心病和高血压疾病的发病率显著高于A组和对照组,比较差异具有统计学意义(P<0.05),A组和B组高血脂发病率均显著高于对照组,比较差异具有统计学意义(P<0.05)。结论:阿尔茨海默病和血管性痴呆均与FPD、IDE以及高血脂有较大关系,高血压、冠心病和糖尿病与血管性痴呆有较大关系。 Objective: To study the relationship between alzheimer's disease, vascular dementia and glucose metabolism and their risk factors. Methods: Selected 80 cases of patients with alzheimer's disease (as A group), 70 cases of patients with vascular dementia(as group B) and another 70 people without dementia (as control group) who were treated in our hospital from December 2013 to December 2014, detected the different index levels of blood glucose in three groups, and analyzed the risk factors for Alzheimer's disease and vascular dementia. Results: Fasting plasma glucose (FPG) of A group and B group were significantly higher than the control group, while the insulin-degrading enzyme ODE) was significantly lower than the control group,the differences were statistically significant(P〈0.05); The incidence of diabetes, coronary heart disease and hypertension of B group were significantly higher than A group and control group, the differences were statistically significant (P〈0.05), and the incidence of high cholesterol of A group and B group were significantly higher than control group, the differences were statistically significant (P〈0.05). Conclusion: FPG, IDE and high cholesterol are greatly related to Alzheimer's disease and vascular dementia, and hypertension, coronary heart disease and diabetes are greatly related to vascular dementia.
出处 《现代生物医学进展》 CAS 2015年第15期2932-2934,共3页 Progress in Modern Biomedicine
关键词 阿尔茨海默病 血管性痴呆 血糖 危险因素 Alzheimer's disease Vascular dementia Blood glucose Risk factors
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  • 1Robbins T W , McAlonan G , Muir J L, et al. Cognitive enhancers in theory and practice studies of the eholinelgic hypothesis of cognitive deficits in Alzheimers disease [ J]. Behav Brain Res, 1997, 83 : 15-23.
  • 2Tohgi H. Remarkable reduction in aeetylcholine concentration in the cerebrospinal fluid from patients with Alzheimer type dementia [J]. Neurooci Lett, 1994, 177 (1):139-142.
  • 3Glenner G G, Wong C W. Alzheimer's disease and Down's syndrome: sharing of a unique cerebrovascular amyloid fibril protein [J]. Biochem Biophys Res Conanun, 1984 , 16; 122 (3): 1131 -1135.
  • 4Masters C L, Simms G, Weinman NA, et, al. Amyloid plaque core protein in Alzheimer disease and Down syndrome [J]. Proc Natl Acad Sci U S A, 1985 , 82 (12) : 4245 -4249.
  • 5Hardy J A , Higgins G A . Alzheimer's disease: the amyloid cascade hypothesis [J]. Science , 1992, 256:184-185.
  • 6Pric DL , Sidia SSW. Mutant genes in familial Alzheimer's disease and transgenic models [ J ] . Annu Rev Neuresci, 1998, 21 (5) : 479 -505.
  • 7Bellucci A, Luccarini I, Scali C, et al. Cholinergic dysfunction, neuronal damage and axonal loss in TgCRND8 mice [J]. Neurobiology of Disease, 2006, 23 (2) : 260-272.
  • 8Barn Bcrger M E, Harris M E, Mcdonald D R, et al. A cell surface receptor complex for fibrilar bata - amyloid mediates micro- glial activation [J]. J Nettroscl, 2003, 23 (7): 2665.
  • 9Bramblett G T, Goedert M, Jakes R, et al. Abnormal tau phosphorylation at Ser396 in Alzheimer's disease recapitulates development and contributes to reduced microtubule hinging [ J]. Neuron, 1993, 10: 1089-1099.
  • 10Mandelkow E M, Mandelkow E. Tau in Alzheimer's disease [J]. Trends Cell Biol, 1998, 8:425 -427.

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