Faster forgetting contributes to impaired spatial memory in the PDAPP mouse: Deficit in memory retrieval associated with increased sensitivity to interference?
Faster forgetting contributes to impaired spatial memory in the PDAPP mouse: Deficit in memory retrieval associated with increased sensitivity to interference?
复制标题
DOI：
10.1101/lm.990208
复制
发表时间：
2008-09-01
影响因子：
2
通讯作者：
Morris, Richard G. M.
中科院分区：
文献类型：
--
作者：
Daumas, Stephanie;Sandin, Johan;Morris, Richard G. M.
进行了两个实验来研究PDAPP小鼠更快遗忘的可能性（正如Games及其同事在早期论文中报道的那样，这是一种成熟的阿尔茨海默病模型）。实验1，使用13-16个月的小鼠，证实了半合子PDAPP小鼠相对于同窝对照在水迷宫中的空间参考记忆任务中存在缺陷。然而，在过度训练到同等导航性能的标准后，一系列记忆保持测试显示PDAPP组的遗忘速度更快。非常有限的再训练足以恢复两组人的良好记忆，这表明他们更快的遗忘可能是由于检索失败而不是痕迹衰减。在实验2中，6月龄的PDAPP和对照组被要求学习一系列空间位置中的每一个，并在学习每个位置后10分钟评估其记忆。PDAPP小鼠最初没有明显的记忆缺陷，但通过一系列位置建立的缺陷表明对干扰的敏感性增加。更快的遗忘和更多的干扰可能都反映了访问记忆痕迹的困难。这种对人类突变APP小鼠认知缺陷的一个方面的解释与在阿尔茨海默病患者中观察到的缺陷相似，进一步支持了该疾病转基因模型的有效性。
Two experiments were conducted to investigate the possibility of faster forgetting by PDAPP mice (a well-established model of Alzheimer's disease as reported by Games and colleagues in an earlier paper). Experiment 1, using mice aged 13-16 mo, confirmed the presence of a deficit in a spatial reference memory task in the water maze by hemizygous PDAPP mice relative to littermate controls. However, after overtraining to a criterion of equivalent navigational performance, a series of memory retention tests revealed faster forgetting in the PDAPP group. Very limited retraining was sufficient to reinstate good memory in both groups, indicating that their faster forgetting may be due to retrieval failure rather than trace decay. In Experiment 2, 6-mo-old PDAPP and controls were required to learn each of a series of spatial locations to criterion with their memory assessed 10 min after learning each location. No memory deficit was apparent in the PDAPP mice initially, but a deficit built up through the series of locations suggestive of increased sensitivity to interference. Faster forgetting and increased interference may each reflect a difficulty in accessing memory traces. This interpretation of one aspect of the cognitive deficit in human mutant APP mice has parallels to deficits observed in patients with Alzheimer's disease, further supporting the validity of transgenic models of the disease.