What is normal in normal aging? Effects of aging, amyloid and Alzheimer's disease on the cerebral cortex and the hippocampus.
What is normal in normal aging? Effects of aging, amyloid and Alzheimer's disease on the cerebral cortex and the hippocampus.
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DOI：
10.1016/j.pneurobio.2014.02.004
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发表时间：
2014-06
影响因子：
6.7
通讯作者：
Walhovd, Kristine B.
中科院分区：
文献类型：
--
作者：
Fjell, Anders M.;McEvoy, Linda;Holland, Dominic;Dale, Anders M.;Walhovd, Kristine B.
关键词：
在正常衰老中可以预期什么，正常衰老在哪里停止，病理性神经变性开始？随着老年痴呆症（如阿尔茨海默病（AD））的缓慢进展，很难区分与年龄相关的变化与未检测到的疾病的影响。本文综述了近年来关于大脑皮层和海马在衰老过程中的变化以及正常衰老与AD之间的界限的研究。我们认为，显着的皮质减少是显而易见的，在老年人的额颞区，即使与AD的概率低，包括重叠的默认模式网络的区域。重要的是，这些区域在AD中显示出高水平的淀粉样蛋白沉积，并且在疾病早期在结构和功能上都是脆弱的。这种正常-病理同源性是理解的关键，因为衰老本身是散发性AD的主要风险因素。因此，这些变化可能是正常衰老的一部分，而不一定反映疾病的早期迹象，并可能说明为什么衰老的大脑比年轻的大脑更容易患AD。我们认为，具有高度终身可塑性的区域容易受到正常衰老的不利影响，并且这种年龄脆弱性使它们更容易受到额外的病理性AD相关变化的影响。我们的结论是，如果不了解为什么它更好地影响老年人的大脑，就很难理解AD，我们需要一个模型，该模型可以解释与AD易感区域年龄相关的变化，而不依赖于AD病理学。
What can be expected in normal aging, and where does normal aging stop and pathological neurodegeneration begin? With the slow progression of age-related dementias such as Alzheimer’s Disease (AD), it is difficult to distinguish age-related changes from effects of undetected disease. We review recent research on changes of the cerebral cortex and the hippocampus in aging and the borders between normal aging and AD. We argue that prominent cortical reductions are evident in fronto-temporal regions in elderly even with low probability of AD, including regions overlapping the default mode network. Importantly, these regions show high levels of amyloid deposition in AD, and are both structurally and functionally vulnerable early in the disease. This normalcy-pathology homology is critical to understand, since aging itself is the major risk factor for sporadic AD. Thus, rather than necessarily reflecting early signs of disease, these changes may be part of normal aging, and may inform on why the aging brain is so much more susceptible to AD than is the younger brain. We suggest that regions characterized by a high degree of life-long plasticity are vulnerable to detrimental effects of normal aging, and that this age-vulnerability renders them more susceptible to additional, pathological AD-related changes. We conclude that it will be difficult to understand AD without understanding why it preferably affects older brains, and that we need a model that accounts for age-related changes in AD-vulnerable regions independently of AD-pathology.
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影响因子：
2.6
作者：
Addis DR;Roberts RP;Schacter DL
通讯作者：
Schacter DL
影响因子：
4
作者：
Arenaza-Urquijo, Eider M.;Molinuevo, Jose-Luis;Bartres-Faz, David
通讯作者：
Bartres-Faz, David
影响因子：
25
作者：
Bero AW;Yan P;Roh JH;Cirrito JR;Stewart FR;Raichle ME;Lee JM;Holtzman DM
通讯作者：
Holtzman DM
影响因子：
16.2
作者：
Andrews-Hanna, Jessica R.;Reidler, Jay S.;Sepulcre, Jorge;Poulin, Renee;Buckner, Randy L.
通讯作者：
Buckner, Randy L.
影响因子：
11.2
作者：
Becker, J. Alex;Hedden, Trey;Carmasin, Jeremy;Maye, Jacqueline;Rentz, Dorene M.;Putcha, Deepti;Fischl, Bruce;Greve, Douglas N.;Marshall, Gad A.;Salloway, Stephen;Marks, Donald;Buckner, Randy L.;Sperling, Reisa A.;Johnson, Keith A.
通讯作者：
Johnson, Keith A.