Early Markers Of Alzheimer Disease

阿尔茨海默病（AD）是主要发生在较晚年龄的几种神经退行性疾病（痴呆）中最普遍的，偶尔在60岁之前，但更频繁地在70岁之后。本研究探讨了前瞻性的心理，神经和神经心理学的变化，参与者从巴尔的摩纵向研究老化（BLSA）。对60岁及以上的参与者进行神经学和神经心理学检查，重复在早期对这些受试者进行的许多测试。可能的阿尔茨海默病的诊断遵循NINCDS-ADRDA标准。此外，本研究还探讨了抑郁症和抑郁症状的作用。这些情况涉及多达一半的痴呆症病例，特别是在早期病例中。虽然目前还不清楚抑郁症是否是统一的前驱症状或危险因素，但重要的是要了解抑郁症状的时间过程及其与认知能力下降和痴呆的关系。 在以人群为基础的痴呆发病率和患病率的流行病学研究中，血管性痴呆被认为是仅次于AD的第二大痴呆病因。大多数研究表明，AD型病理和血管病变对痴呆的诊断有独立的贡献。由于血管和AD病理共存于许多老年受试者的大脑中，因此研究每个过程对痴呆临床表现的独特贡献一直具有挑战性。部分研究人员使用来自巴尔的摩老龄化纵向研究（BLSA）尸检项目的临床数据，研究了临床上明显的中风对痴呆风险的影响，该项目是一项前瞻性研究，研究了社区居住志愿者死亡后同意尸检的正常衰老的影响。我们使用来自335名BLSA参与者的前瞻性数据，研究了临床可检测到的中风对痴呆风险的影响。临床上明显的卒中在我们的队列中很常见（90岁时的累积风险为15.4%; 95% CI 10-22%），与未发生卒中的受试者相比，具有显著的痴呆风险（OR = 5.55; 95% CI 2.76-11.4）。中风的大小，通过中风后临床缺陷来衡量，在随后变得痴呆的那组和没有中风的那组之间没有差异。大多数中风后痴呆的参与者在中风前有轻度认知障碍的证据（19人中的14人）。此外，临床症状性卒中是轻度认知功能障碍转化为痴呆的主要危险因素（OR 12.4; 95% C.I. 1.5 ? 99）。当中风前没有认知障碍时，随后痴呆的风险不会增加。在没有中风的情况下，其他动脉粥样硬化性疾病的病史不会导致痴呆。这些数据表明，中风后痴呆通常是由中风前出现的认知障碍决定的。 在一项单独的研究中，部分调查人员检查了流行病学研究中心抑郁量表的4个抑郁症量表的横截面和纵向年龄和性别差异。两项独立研究（样本1 = 2，076;样本2 = 943）用于确定结果的稳定性。样本1来自全国健康和营养调查基线和后续研究，其中对1 167名妇女和909名男子的全国代表性样本进行了6至10年的检查。样本2来自BLSA，其中400名女性和543名男性在8年内接受了检查。结果表明，70岁以下成年人的稳定程度合理。然而，在大约70岁之后，躯体症状和缺乏幸福感的年龄相关性显著增加，而与抑郁情绪和人际关系问题相关的症状保持稳定。值得注意的是，抑郁情绪症状保持稳定，考虑到显着的年龄相关的躯体变化。在分析中增加共病的身体疾病并没有减少年龄和抑郁症状之间的关联，这表明部分关联并没有被身体健康所充分解释。

Alzheimer's disease (AD) is the most widespread among several neurological degenerative diseases (dementias) that occur principally at later ages, occasionally before 60, but more frequently after age 70. This study examines prospective psychological, neurological, and neuropsychological changes in participants from the Baltimore Longitudinal Study of Aging (BLSA). Neurological and neuropsychological examinations are administered to participants aged 60 and older, repeating many of the tests that were administered to these subjects at earlier ages. Diagnoses of probable Alzheimer's disease follow the NINCDS-ADRDA criteria. In addition, this study examines the role of depression and depressive symptoms. These conditions are involved in as many as half of dementia cases, particularly in the early cases. Although it is unclear whether depression is uniformly prodromal or a risk factor, it is important to understand the time course of depressive symptoms and its association with cognitive decline and dementia. Vascular dementia is considered second only to AD as a cause of dementia in population-based epidemiological studies of the incidence and prevalence of dementia. Most studies indicate that AD type pathology and vascular disease make independent contributions to the diagnoses of dementia. Because vascular and AD pathology coexist in the brains of many elderly subjects, it has been challenging to examine the unique contribution of each process to the clinical picture of dementia. Section investigators examined the effect of clinically overt stroke on the risk of dementia using clinical data from the Baltimore Longitudinal Study of Aging (BLSA) Autopsy Program, a prospective study of the effects of normal aging in community-dwelling volunteers who have agreed to autopsy following death. We examined the effect of a clinically detectable stroke on the risk of dementia using prospective data from 335 BLSA participants. Clinically overt strokes are common in our cohort (cumulative risk by age 90 15.4%; 95% CI 10-22%) and confer a significant risk for dementia compared to subjects without stroke (OR = 5.55; 95% CI 2.76-11.4). The size of the stroke, measured by the post-stroke clinical deficit, was not different in the group who subsequently became demented from that in the group with stroke who did not. The majority of participants who became demented after a stroke had evidence of mild cognitive impairment preceding the stroke (14 of 19). Moreover, a clinically symptomatic stroke was a major risk factor for the conversion of mild cognitive impairment to dementia (OR 12.4; 95% C.I. 1.5 ? 99). When cognitive impairment did not precede the stroke, there was no increase in the risk of subsequent dementia. A history of other atherosclerotic diseases in the absence of stroke did not contribute to dementia. These data suggest that dementia after stroke is often determined by cognitive impairment that existeed prior to the stroke. In a separate study, section investigators examined cross-sectional and longitudinal age and sex differences in each of the Center for Epidemiological Studies Depression Scale's 4 subscales of depressive symptomatology. Two independent studies (Sample 1 = 2,076; Sample 2 = 943) were used for purposes of establishing stability of findings. Sample 1 was derived from the National Health and Nutrition Survey baseline and follow-up study in which a nationally representative sample of 1,167 women and 909 men were examined over 6-10 years. Sample 2 was derived from the BLSA in which 400 women and 543 men were examined over 8 years. Results indicate a reasonable degree of stability among adults under 70 years of age. However, there were significant age-related increases in somatic symptoms and lack of well-being after approximately 70 years of age, whereas symptoms related to depressed affect and interpersonal problems remained stable. Notably, depressive affect symptoms remained stable given significant age-related somatic changes. The addition of comorbid physical illness to the analysis did not reduce the association between age and depressive symptoms, indicating that part of the association was not substantially accounted for by physical health.