PREVALENCE AND SPECTRUM OF B12 DEFICIENCY IN THE AGED

老年痴呆症对人类和人类来说都是一种高昂的代价 痛苦和医疗保健费用是造成 老年人口的就业能力和独立生活。一直以来 多年来一直知道维生素B12(钴胺)缺乏会导致 痴呆和其他难以区分的神经行为症状 患有阿尔茨海默氏症。采用特定技术的前瞻性研究 钴胺缺乏症的诊断方法研究 痴呆症是必要的。这项提案计划确定 下列组患者的钴胺缺乏症：1)未选择 老年患者；2)出现记忆和运动障碍的患者 诊所；3)住进国立精神病院的病人；4)居民 疗养院。灵敏和特异的气相色谱/质谱仪 血清甲基丙二酸和同型半胱氨酸的光谱分析 与两种人类钴胺依赖酶相关的代谢物将是 用于确认低血钴素患者的组织缺陷 级别。一组老年患者和一组痴呆症患者 被发现血清钴胺水平较低的人将被招募两个 前瞻性研究评估血液学、神经学、 放射学、脑电和神经心理学异常 在基线以及父母出生8周、6个月和1岁后出现 钴胺疗法。这些研究中的低血钴胺患者 甲基丙二酸和/或同型半胱氨酸水平升高 与血清钴胺水平较低和正常的患者比较 代谢产物和一组年龄和性别匹配的对照组患者 无痴呆或钴胺缺乏症。高血压病的流行 将评估患者的脑脊液甲基丙二酸水平 血清钴胺水平也很低。该项目旨在 确定具有生物化学意义的钴胺缺乏症的患病率 在老年人群和患有神经学或精神病学疾病的患者中 异常现象。此外，在两个亚组的患者中， 神经行为异常的定义将使用敏感、多方面的 方法，以及对钴胺治疗的反应的性质和程度 将会被确定。

Dementing disorders in the elderly exact a high cost in both human suffering and health care dollars and are the leading cause of the loss of employability and independent living in the older population. It has been known for many years that vitamin B12 (cobalamin) deficiency can cause dementia and other neurobehavioral symptoms which are indistinguishable from Alzheimer's disease. Prospective studies which employ specific methods of diagnosis investigating the role of cobalamin deficiency in dementia are needed. This proposal plans to determine the prevalence of cobalamin deficiency in the following groups of patients: 1) Unselected elderly patients; 2) patients presenting to memory and movement disorders clinics; 3) patients admitted to state mental hospitals; and 4) residents of nursing homes. Sensitive and specific gas chromatography/mass spectrometry assays for serum methylmalonic acid and homocysteine, two metabolites related to the two human cobalamin-dependent enzymes, will be used to confirm tissue deficiency in patients with low serum cobalamin levels. A group of elderly patients and a group of demented patients who are found to have low serum cobalamin levels will be recruited for two prospective studies which evaluate the pattern of hematologic, neurologic, radiographic, electroencephalographic and neuropsychological abnormalities present at baseline and after 8 weeks, 6 months and 1 year of parental cobalamin therapy. The patients in these studies with low serum cobalamin levels and elevated methylmalonic acid and/or homocysteine levels will be compared to the patients with low serum cobalamin levels and normal metabolites and to a group of control patients matched for age and sex without dementia or cobalamin deficiency. The prevalence of elevated cerebrospinal fluid methylmalonic acid levels will be evaluated in patients with low serum cobalamin levels also. This project is designed to determine the prevalence of biochemically significant cobalamin deficiency in elderly populations and patients with neurologic or psychiatric abnormalities. In addition, in two subsets of patients, the pattern of neurobehavioral abnormalities will be defined using sensitive, multifaceted methodology, and the nature and extent of response to cobalamin therapy will be determined.