As well known that synapse loss is a significant pathological feature of Alzheimer’s disease (AD), meanwhile, the hippocampus is one of brain regions to be first affected in the early stage of AD. Thus, this work employs a comprehensive DG-CA3 network model of the hippocampus so as to explore the neuronal correlation between glutamatergic synapse loss and abnormal firing rhythm associated with AD from the perspective of neurocomputation. The neuropathological condition of glutamatergic synapse loss caused by the reduction of Shank3 protein in AD patients is imitated by decreasing glutamatergic excitatory synapse strength between different neurons. By means of power spectral analysis and dynamics technique, the numerical results reveal that excitability of pyramidal neuron as well as oriens lacunosum-moleculare (O-LM) cell in CA3 region is strongly degraded by the decrease of NMDA or AMPA-type glutamatergic excitatory synapse strength. Moreover, the relative power together with the peak of relative power density within alpha band is also diminished by decreasing glutamatergic synapse strength. These findings accord with the electrophysiological experiment of EEG that there is a decrease of alpha rhythm for AD patients, on the same time, they could highlight the significance of glutamatergic synapse loss in the pathogenesis of AD.

众所周知，突触缺失是阿尔茨海默病（AD）的一个重要病理特征，同时，海马区是AD早期最先受累的脑区之一。因此，本工作采用海马的综合 DG-CA3 网络模型，从神经计算的角度探讨与 AD 相关的谷氨酸能突触丢失与异常放电节律之间的神经元相关性。AD 患者由于 Shank3 蛋白减少引起的谷氨酸能突触丢失的神经病理学状况是通过降低不同神经元之间的谷氨酸能兴奋性突触强度来模拟的。通过功率谱分析和动力学技术，数值结果表明，随着NMDA或AMPA型谷氨酸能兴奋性突触强度的降低，CA3区锥体神经元和腔隙分子（O-LM）细胞的兴奋性明显降低。此外，随着谷氨酸能突触强度的降低，α波段内的相对功率和相对功率密度的峰值也会降低。这些发现与脑电图电生理实验表明AD患者存在α节律降低，同时也可以突出谷氨酸能突触缺失在AD发病机制中的意义。通过降低谷氨酸能突触强度，α带内的相对功率以及相对功率密度的峰值也降低了。这些发现与脑电图电生理实验表明AD患者存在α节律降低，同时也可以突出谷氨酸能突触缺失在AD发病机制中的意义。通过降低谷氨酸能突触强度，α带内的相对功率以及相对功率密度的峰值也降低了。这些发现与脑电图电生理实验表明AD患者存在α节律降低，同时也可以突出谷氨酸能突触缺失在AD发病机制中的意义。