ArticleCognitive neurodynamics2022
How glutamatergic synapse loss affects the firing rhythm of DG-CA3 model related with Alzheimer's disease.
Article in Cognitive neurodynamics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 12 citations in OpenAlex.
- The relationship between cortical synaptic terminal density marker SV2A and glutamate early in the course of schizophrenia: a multimodal PET and MRS imaging study.Translational psychiatry · 2025Article
- Complexity decline of hippocampal CA1 circuit model due to cholinergic deficiency associated with Alzheimer's disease.Cognitive neurodynamics · 2024Article
- Marine Sources of DHA-Rich Phospholipids with Anti-Alzheimer Effect.Marine drugs · 2022Review
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3 authors at 2 institutions in 1 country.
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Abstract
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.
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