Aging-associated changes in human brain
Aging-associated changes in human brain
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DOI：
10.1097/00005072-199712000-00001
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发表时间：
1997-12-01
影响因子：
3.2
通讯作者：
Graham, DI
中科院分区：
文献类型：
--
作者：
Mrak, RE;Griffin, WST;Graham, DI
老年人的大脑中常见多种解剖学和组织学改变。然而，识别内在的衰老变化（与累积环境损害引起的变化不同）是有问题的。一定程度的神经元和体积损失似乎是不可避免的，但最近的研究表明，这种变化的幅度比以前想象的要小得多，而且对认知完整个体的树突复杂性的研究表明，神经元可塑性持续到八个十年。随着年龄的增长，许多血管变化变得更加频繁，其中许多归因于高血压和动脉粥样硬化等全身性疾病。与这些病症没有明显联系的年龄相关血管变化包括在颅内小血管中形成动脉迂曲的透明动脉硬化变化以及被称为“脑白质疏松”的深部大脑白质的放射学变化。衰老伴随着神经胶质细胞活化、蛋白质和脂质氧化损伤、不可逆蛋白质糖化以及DNA损伤的增加，并且这些变化可能部分是与年龄相关的“退行性”病症发生率增加的基础。如阿尔茨海默病和帕金森病。少数组织学变化似乎在老年人大脑中普遍存在。这些包括血脑或脑脊液-脑界面附近的星形细胞过程中淀粉体数量的增加，“老化”色素脂褐质在所有大脑区域的积累，以及颞叶内侧结构中出现阿尔茨海默型神经原纤维缠结（但不一定是淀粉样斑块）。
A wide variety of anatomic and histological alterations are common in brains of aged individuals. However, identification of intrinsic aging changes-as distinct from changes resulting from cumulative environmental insult-is problematic. Some degree of neuronal and volume loss would appear to be inevitable, but recent studies have suggested that the magnitudes of such changes are much less than previously thought, and studies of dendritic complexity in cognitively intact individuals suggest continuing neuronal plasticity into the eighth decade. A number of vascular changes become more frequent with age, many attributable to systemic conditions such as hypertension and atherosclerosis. Age-associated vascular changes not clearly linked to such conditions include hyaline arteriosclerotic changes with formation of arterial tortuosities in small intracranial vessels and the radiographic changes in deep cerebral white matter known as "leukoaraiosis," Aging is accompanied by increases in glial cell activation, in oxidative damage to proteins and lipids, in irreversible protein glycation, and in damage to DNA, and such changes may underlie in part the age-associated increasing incidence of "degenerative" conditions such as Alzheimer disease and Parkinson disease. A small number of histological changes appear to be universal in aged human brains. These include increasing numbers of corpora amylacea within astrocytic processes near blood-brain or cerebrospinal fluid-brain interfaces, accumulation of the "aging" pigment lipofuscin in all brain regions, and appearance of Alzheimer-type neurofibrillary tangles (but not necessarily amyloid plaques) in mesial temporal structures.