Background: Clinical evidence indicates that patients affected by Alzheimer's Disease (AD) fail to form new memories although their memories for old events are intact. This amnesic pattern depends on the selective vulnerability to AD-neurodegeneration of the hippocampus, the brain region that sustains the formation of new memories, while cortical regions that store remote memories are spared.

Objective: To identify the cellular mechanisms underlying impaired recent memories and intact remote memories in a mouse model of AD.

Methods: Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and anterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected to the Contextual Fear Conditioning (CFC) task or in naïve conditions.

Results: We identified a deficit in the formation of recent memories, but not in the recall of remote ones, in Tg2576 mice. With electrophysiological recordings, we detected CFC-induced modifications of the AMPA/NMDA ratio in CA1 pyramidal cells of Wt, but not Tg2576, mice one day after training. CFC-induced changes in the AMPA/NMDA ratio were also detected in the aCC of both Wt and Tg2576 mice 8 days after training.

Conclusion: Our data suggest that in the early AD stages synaptic plasticity of CA1 synapses, crucial to form new memories, is lost, while plasticity of aCC synapses is intact and contributes to the persistence of long-term memories.

中文翻译：

---

阿尔茨海默氏病小鼠模型中顺行性失忆和完整逆行记忆的突触相关。

背景：临床证据表明，受阿尔茨海默氏病（AD）影响的患者虽然对旧事件的记忆完好无损，却无法形成新的记忆。这种记忆删除模式取决于对海马区AD神经神经变性的选择性脆弱性，海马区是维持新记忆形成的大脑区域，而存储远程记忆的皮质区域则被保留。

目的：确定AD小鼠模型中受损的近期记忆和完整的远程记忆的潜在细胞机制。

方法：通过膜片钳记录AD样Tg2576小鼠的急性海马和前扣带回皮层（aCC）切片以及经受情境恐惧条件（CFC）任务或处于幼稚条件下的野生型（Wt）同窝仔的谷氨酸能突触电流。 。

结果：我们在Tg2576小鼠中发现了近期记忆形成的缺陷，但没有发现远处记忆的缺陷。通过电生理学记录，我们在训练后一天检测到了Wt的CA1锥体细胞中CFC诱导的AMPA / NMDA比值的修饰，而Tg2576的小鼠中没有。训练后8天，在Wt和Tg2576小鼠的aCC中也检测到了CFC诱导的AMPA / NMDA比值的变化。

结论：我们的数据表明，在AD早期，CA1突触对形成新记忆至关重要的突触可塑性丧失，而aCC突触的可塑性却完好无损，并有助于长期记忆的持久性。