PREVALENCE AND SPECTRUM OF B12 DEFICIENCY IN THE AGED

描述(研究人员摘要)：；老年人的痴呆障碍 在人类痛苦和医疗保健方面都付出了高昂的代价，而且 在中国失去就业能力和独立生活的主要原因 老年人口。多年来，人们已经知道维生素B12 (钴胺)缺乏可导致痴呆和其他神经行为 与阿尔茨海默氏症难以区分的症状。预期 使用特定诊断方法调查其作用的研究 痴呆症患者的钴胺缺乏症是必要的。这项提案计划 确定下列人群中钴胺缺乏症的患病率 患者：1)未选定的老年患者；2)出现 记忆和运动障碍诊所；3)精神状态患者 医院；4)养老院的居民。灵敏而特异的气体 血清甲基丙二酸和甲基丙二酸的色质联用分析 同型半胱氨酸，两种与人类钴胺依赖相关的代谢物 酶，将被用来确认低血糖患者的组织缺陷 血清钴胺水平。一组老年患者和一组 被发现血清钴胺水平较低的痴呆症患者 被招募参加两项前瞻性研究，评估 血液学、神经学、放射学、脑电图学和 在基线和8周后，6 几个月和一年的非肠道钴胺治疗。住在这里的病人 血清钴胺水平降低和甲基丙二酸升高的研究 和/或同型半胱氨酸水平将与血清水平低的患者进行比较 钴胺水平和正常代谢物以及一组对照患者 年龄和性别匹配，无痴呆症或钴胺缺乏。这个 脑脊液甲基丙二酸水平升高的患病率将 在血清钴胺水平较低的患者中也可进行评估。这 该项目旨在确定生化疾病的流行率 老年人群和慢性支气管炎患者中的钴胺严重缺乏 神经学或精神病学异常。此外，在两个子集中 患者，神经行为异常的模式将被定义 使用敏感的多方面方法，以及 对钴胺治疗的反应将被确定。

DESCRIPTION (Investigator's Abstract):; 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 with memory and movement disorders clinics; 3) patients admitted to state mental hospitals; 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 one year of parenteral 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 an elderly population 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.