Bezdicek Ondrej, Ballarini Tommaso, Buschke Herman, Růžička Filip, Roth Jan, Albrecht Franziska, Růžička Evžen, Mueller Karsten, Schroeter Matthias L, Jech Robert
Department of Neurology and Centre of Clinical Neuroscience.
Max Planck Institute for Human Cognitive and Brain Sciences.
Neuropsychology. 2019 Mar;33(3):391-405. doi: 10.1037/neu0000503.
Our study explored the retrieval deficit and the associative deficit hypotheses of memory impairments in Parkinson's disease (PD). The former supports a memory deficit mediated by attention/executive dysfunctions, whereas the latter hypothesizes a hippocampal memory impairment in PD.
We studied 31 controls and 34 PD patients classified as PD with normal cognition (PD-NC; n = 18) and PD with mild cognitive impairment (PD-MCI; n= 16). To test the retrieval deficit hypothesis, we measured the performance in encoding, retention, and recognition in verbal and visual domains; to test the associative deficit hypothesis, we used a specific associative binding measure. Using resting-state functional-MRI, we compared the functional connectivity of different hippocampal subfields between PD patients and controls, and we related it to memory performance.
Consistently with the retrieval deficit hypothesis, PD-MCI, and PD-NC, were impaired in free recall encoding and retention in comparison to controls, especially in the visual domain. However, as predicted by the associative deficit hypothesis, PD-MCI and, to a lesser extent, PD-NC, showed also significant associative and binding deficits in cued recall. Notably, PD patients compared to controls did not show structural differences, although they had lower connectivity between the anterior hippocampi and the precuneus/superior parietal cortex. Worse performance in memory was associated with a more severe disruption of the hippocampal connectivity.
The pervasive pattern of memory impairment in PD supports both hypotheses. The interplay between the hippocampus, related to associative memory deficits, and the precuneus, related to attentional control, provides a neural signature that reconciles them. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
我们的研究探讨了帕金森病（PD）记忆障碍的检索缺陷和联想缺陷假说。前者支持由注意力/执行功能障碍介导的记忆缺陷，而后者则假设PD存在海马记忆损伤。
我们研究了31名对照者和34名PD患者，这些患者被分类为认知正常的PD（PD-NC；n = 18）和轻度认知障碍的PD（PD-MCI；n = 16）。为了检验检索缺陷假说，我们测量了言语和视觉领域的编码、保持和识别表现；为了检验联想缺陷假说，我们使用了一种特定的联想绑定测量方法。使用静息态功能磁共振成像，我们比较了PD患者和对照者不同海马亚区的功能连接，并将其与记忆表现相关联。
与检索缺陷假说一致，与对照者相比，PD-MCI和PD-NC在自由回忆编码和保持方面受损，尤其是在视觉领域。然而，正如联想缺陷假说所预测的，PD-MCI以及程度较轻的PD-NC在线索回忆中也表现出显著的联想和绑定缺陷。值得注意的是，与对照者相比，PD患者没有显示出结构差异，尽管他们前海马与楔前叶/顶上叶皮质之间的连接性较低。记忆表现较差与海马连接性的更严重破坏有关。
PD中普遍存在的记忆障碍模式支持这两种假说。与联想记忆缺陷相关的海马和与注意力控制相关的楔前叶之间的相互作用提供了一种将它们统一起来的神经特征。（PsycINFO数据库记录（c）2019美国心理学会，保留所有权利）
