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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Hippocampal hyperactivation associated with cortical thinning in Alzheimer's disease signature regions in non-demented elderly adults.
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Hippocampal hyperactivation associated with cortical thinning in Alzheimer's disease signature regions in non-demented elderly adults.

机译：非痴呆老年人的海马过度激活与阿尔茨海默氏病特征区域的皮质变薄有关。

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摘要

Alzheimer's disease (AD) is associated with functional and structural alterations in a distributed network of brain regions supporting memory and other cognitive domains. Functional abnormalities are present in mild cognitive impairment (MCI) with evidence of early hyperactivity in medial temporal lobe regions, followed by failure of hippocampal activation as dementia develops. Atrophy in a consistent set of cortical regions, the "cortical signature of AD," has been reported at the stage of dementia, MCI, and even in clinically normal (CN) older individuals predicted to develop AD. Despite multiple lines of evidence for each of these findings, the relationship between this structural marker of AD-related neurodegeneration and this functional marker of the integrity of the episodic memory system has not yet been elucidated. We investigated this relationship in 34 nondemented older humans (CN, N = 18; MCI, N = 16). Consistent with previous studies, we found evidence of hippocampal hyperactivation in MCI compared with CN. Additionally, within this MCI group, increased hippocampal activation correlated with cortical thinning in AD-signature regions. Even within the CN group, increased hippocampal activity was negatively correlated with cortical thinning in a subset of regions, including the superior parietal lobule (r = -0.66; p < 0.01). These findings, across a continuum of nondemented and mildly impaired older adults, support the hypothesis that paradoxically increased hippocampal activity may be an early indicator of AD-related neurodegeneration in a distributed network.
机译：阿尔茨海默氏病（AD）与支持记忆和其他认知域的大脑区域分布网络中的功能和结构改变有关。功能异常存在于轻度认知障碍（MCI）中，并有颞颞内侧区域早期活动亢进的证据，随后随着痴呆的发展海马激活失败。据报道，在痴呆，MCI阶段，甚至在预计发展为AD的临床正常（CN）老年人中，一致的皮质区域都出现了萎缩，即“ AD的皮质特征”。尽管这些发现中的每一个都有多方面的证据，但尚未阐明该AD相关神经退行性变的结构标志物与该事件记忆系统完整性的功能性标志物之间的关系。我们在34位无痴呆的老年人中调查了这种关系（CN，N = 18; MCI，N = 16）。与以前的研究一致，我们发现与CN相比，MCI中海马过度活化的证据。此外，在这个MCI组中，海马激活增加与AD签名区域的皮质变薄相关。即使在CN组内，海马活动的增加与一部分区域的皮质变薄也呈负相关，包括上顶叶（r = -0.66; p <0.01）。这些发现在连续的未痴呆和轻度受损的成年人中，支持以下假设：反常增加的海马活动可能是分布式网络中AD相关神经变性的早期指标。

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