Teipel Stefan J, Schapiro Mark B, Alexander Gene E, Krasuski Jack S, Horwitz Barry, Hoehne Christian, Möller Hans-Jürgen, Rapoport Stanley I, Hampel Harald
Alzheimer Memorial Center and Geriatric Psychiatry Branch, Ludwig-Macimilian University, Munich, Germany.
Am J Psychiatry. 2003 Oct;160(10):1870-8. doi: 10.1176/appi.ajp.160.10.1870.
Aging in Down's syndrome is accompanied by amyloid and neurofibrillary pathology, the regional and laminar distribution of which resembles pathological changes seen in Alzheimer's disease. Previous studies using magnetic resonance imaging (MRI) demonstrated age-related atrophy of medial temporal lobe structures in nondemented older subjects with Down's syndrome, reflecting early allocortical pathology. Corpus callosum atrophy has been established as a marker of neocortical neuronal loss in Alzheimer's disease. This study investigated whether atrophy of the corpus callosum and hippocampus occurs in nondemented subjects with Down's syndrome and compared the degree of age-related atrophy between these structures.
Hippocampus and corpus callosum measures were obtained from volumetric T(1)-weighted MRI scans of 34 nondemented Down's syndrome adults (mean age=41.6 years, 17 women) and 31 healthy comparison subjects (mean age=41.8 years, 14 women).
Down's syndrome subjects had smaller corpus callosum areas and hippocampal volumes relative to age-matched healthy comparison subjects, even after age and total intracranial volume were controlled. There was an age-related decrease of corpus callosum area (most prominent in posterior regions) and hippocampal volume in the Down's syndrome group. The degree of the age effect was comparable between the total corpus callosum and hippocampus, and corpus callosum size was correlated with cognitive performance in the Down's syndrome subjects. There was no correlation between age and corpus callosum or hippocampal size in the comparison group.
Comparable decrease of corpus callosum and hippocampal size with age in nondemented subjects with Down's syndrome suggests that neocortical neuronal alterations accompany allocortical changes in the predementia phase of Down's syndrome.
唐氏综合征患者的衰老伴有淀粉样蛋白和神经原纤维病变,其区域和层状分布类似于阿尔茨海默病所见的病理变化。以往使用磁共振成像(MRI)的研究表明,非痴呆的老年唐氏综合征患者内侧颞叶结构存在与年龄相关的萎缩,反映了早期原皮质病变。胼胝体萎缩已被确立为阿尔茨海默病新皮质神经元丢失的标志物。本研究调查了非痴呆唐氏综合征患者是否存在胼胝体和海马萎缩,并比较了这些结构中与年龄相关的萎缩程度。
从34名非痴呆唐氏综合征成年人(平均年龄=41.6岁,17名女性)和31名健康对照者(平均年龄=41.8岁,14名女性)的容积性T(1)加权MRI扫描中获取海马和胼胝体测量数据。
即使在控制了年龄和总颅内体积后,唐氏综合征患者的胼胝体面积和海马体积相对于年龄匹配的健康对照者仍较小。唐氏综合征组中,胼胝体面积(最明显的是后部区域)和海马体积随年龄增长而减小。胼胝体总体和海马的年龄效应程度相当,且唐氏综合征患者的胼胝体大小与认知表现相关。对照组中年龄与胼胝体或海马大小之间无相关性。
非痴呆唐氏综合征患者胼胝体和海马大小随年龄出现类似程度的减小,这表明在唐氏综合征的痴呆前期,新皮质神经元改变伴随着原皮质变化。