Visual short-term memory deficits associated with GBA mutation and Parkinson's disease.
Visual short-term memory deficits associated with GBA mutation and Parkinson's disease.
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DOI：
10.1093/brain/awu143
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发表时间：
2014-08
期刊：
影响因子：
--
通讯作者：
Husain M
中科院分区：
文献类型：
--
作者：
Zokaei N;McNeill A;Proukakis C;Beavan M;Jarman P;Korlipara P;Hughes D;Mehta A;Hu MT;Schapira AH;Husain M
溶酶体酶葡萄糖脑苷脂酶（GBA）基因突变的个体患帕金森病并伴有认知缺陷的风险极高。我们检查了长期与帕金森病患者相关的视觉短期记忆障碍是否也存在于 GBA 阳性个体（无论患有或不患有帕金森病）中。视觉工作记忆的精确度是通过一系列顺序任务来测量的，其中参与者观察四个条，每个条具有不同的颜色和方向，并按顺序呈现在屏幕中心。之后，他们被要求调整彩色探针条的方向，以匹配序列中相同颜色探针条的方向。另一种注意力“过滤”条件测试了患者选择性编码四个条形之一而忽略其他条形的能力。使用针对知觉和运动因素控制的相同刺激的感觉运动任务。与健康对照相比，GBA 阳性个体（无论是否患有帕金森病）以及 GBA 阴性帕金森病患者的记忆精确度均存在显着缺陷。最糟糕的记忆发生在患有帕金森病的 GBA 阳性病例中。尽管所有组的视觉短期记忆均受损，但与 GBA 突变和帕金森病相关的错误来源之间存在双重分离。 GBA 阳性个体中观察到的缺陷，无论他们是否患有帕金森病，都可以通过记忆中其他项目特征的干扰系统性增加来解释：错误绑定错误。相比之下，帕金森病患者的损伤，无论 GBA 状态如何，都是通过随机反应增加来解释的。 GBA 阳性且患有帕金森病的个体会犯两种类型的错误，表现最差。这些发现为与 GBA 突变和帕金森病相关的视觉短期记忆领域内的可分离特征缺陷提供了证据。识别 GBA 突变与帕金森病中认知障碍的具体模式可能很重要，因为它可能有助于识别有患帕金森病风险的个体。
Individuals with mutation in the lysosomal enzyme glucocerebrosidase (GBA) gene are at significantly high risk of developing Parkinson’s disease with cognitive deficit. We examined whether visual short-term memory impairments, long associated with patients with Parkinson’s disease, are also present in GBA-positive individuals—both with and without Parkinson’s disease. Precision of visual working memory was measured using a serial order task in which participants observed four bars, each of a different colour and orientation, presented sequentially at screen centre. Afterwards, they were asked to adjust a coloured probe bar’s orientation to match the orientation of the bar of the same colour in the sequence. An additional attentional ‘filtering’ condition tested patients’ ability to selectively encode one of the four bars while ignoring the others. A sensorimotor task using the same stimuli controlled for perceptual and motor factors. There was a significant deficit in memory precision in GBA-positive individuals—with or without Parkinson’s disease—as well as GBA-negative patients with Parkinson’s disease, compared to healthy controls. Worst recall was observed in GBA-positive cases with Parkinson’s disease. Although all groups were impaired in visual short-term memory, there was a double dissociation between sources of error associated with GBA mutation and Parkinson’s disease. The deficit observed in GBA-positive individuals, regardless of whether they had Parkinson’s disease, was explained by a systematic increase in interference from features of other items in memory: misbinding errors. In contrast, impairments in patients with Parkinson’s disease, regardless of GBA status, was explained by increased random responses. Individuals who were GBA-positive and also had Parkinson’s disease suffered from both types of error, demonstrating the worst performance. These findings provide evidence for dissociable signature deficits within the domain of visual short-term memory associated with GBA mutation and with Parkinson’s disease. Identification of the specific pattern of cognitive impairment in GBA mutation versus Parkinson’s disease is potentially important as it might help to identify individuals at risk of developing Parkinson’s disease.
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影响因子：
14.5
作者：
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通讯作者：
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