Recently, we have reported that dentate mossy cells (MCs) control memory precision via directly and functionally innervating local somatostatin (SST) inhibitory interneurons. Here, we report a discovery that dysfunction of synaptic transmission between MCs and SST cells causes memory imprecision in a mouse model of early Alzheimer's disease (AD). Single‐cell RNA sequencing reveals that miR‐128 that binds to a 3′UTR of STIM2 and inhibits STIM2 translation is increasingly expressed in MCs from AD mice. Silencing miR‐128 or disrupting miR‐128 binding to STIM2 evokes STIM2 expression, restores synaptic function, and rescues memory imprecision in AD mice. Comparable findings are achieved by directly engineering MCs with the expression of STIM2. This study unveils a key synaptic and molecular mechanism that dictates how memory maintains or losses its details and warrants a promising target for therapeutic intervention of memory decays in the early stage of AD.

中文翻译：

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苔藓细胞突触功能障碍在阿尔茨海默氏病小鼠模型中通过miR-128抑制STIM2导致记忆不精确。

最近，我们已经报道，齿状苔藓细胞（MCs）通过直接和功能上支配局部生长抑素（SST）抑制性神经元来控制记忆的精度。在这里，我们报告一个发现，在早期阿尔茨海默氏病（AD）小鼠模型中，MC和SST细胞之间的突触传递功能障碍导致记忆不精确。单细胞RNA测序揭示，与AD2小鼠的MC越来越表达与STIM2的3'UTR结合并抑制STIM2翻译的miR-128。沉默miR-128或破坏miR-128与STIM2的结合会唤起STIM2表达，恢复突触功能，并挽救AD小鼠的记忆障碍。通过直接工程改造具有STIM2表达的MC，可以实现可比的发现。