PREVALENCE AND SPECTRUM OF B12 DEFICIENCY IN THE AGED

描述（研究者摘要）：老年痴呆症 在人类痛苦和医疗保健方面都付出了高昂的代价， 就业能力和独立生活能力丧失的主要原因， 老年人口。 多年来，人们一直知道维生素B12 （钴胺素）缺乏可导致痴呆和其他神经行为 这些症状与阿尔茨海默氏病难以区分。 前瞻性 采用特定诊断方法的研究 维生素B12缺乏症的治疗方法。 该提案计划 确定以下人群中钴胺素缺乏症的患病率： 患者：1）未选择的老年患者; 2）表现为 记忆和运动障碍诊所; 3）精神状态患者 医院; 4）疗养院的居民。 敏感性和特异性气体 血清甲基丙二酸的色谱/质谱分析， 同型半胱氨酸，两种代谢物相关的两个人钴胺素依赖 酶，将用于确认组织缺乏症患者低 血清钴胺素水平 一组老年患者和一组 被发现血清钴胺素水平低的痴呆患者将被 招募了两个前瞻性研究，评估模式， 血液学、神经学、放射学、脑电图和 基线和8周后存在神经心理学异常，6 月和一年的非肠道钴胺素治疗。 这些病人 血清钴胺素水平低和甲基丙二酸升高的研究 和/或同型半胱氨酸水平将与具有低血清 钴胺素水平和正常代谢物，并对一组对照患者 年龄和性别匹配，没有痴呆症或钴胺素缺乏症。 的 脑脊液甲基丙二酸水平升高的患病率将 在血清钴胺素水平低的患者中也进行评估。 这 该项目旨在确定生物化学 在老年人群和患有 神经或精神异常。 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， 将确定对钴胺素治疗的反应。

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.