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<p>Although β-amyloid (Aβ) accumulation is a cardinal pathological hallmark of Alzheimer’s disease (AD), it also critically disrupts synchronized activity in glia-neuronal motifs—an electrophysiological manifestation closely associated with cognitive decline. This dysfunction stems from Aβ-induced neuroinflammation and impaired synaptic plasticity. To investigate this, we present a multi-scale coupled heterogeneous astrocyte-neuronal model that comprises a Hindmarsh-Rose (HR) pyramidal neuron, a Morris-Lecar (ML) interneuron, and an astrocyte to explore the electrical activity within a minimal glia-neuronal motif. This model dynamically simulates, through astrocyte, the positive feedback of endoplasmic reticulum calcium leakage and mitochondrial calcium overload triggered by β-amyloid protein (βAP), while regulates synaptic plasticity in real time through glial neurotransmitter release. Meanwhile, a memristor is employed to model the non-monotonic attenuation of synaptic weights and the resultant imbalance between long-term potentiation (LTP) and long-term depression (LTD) that occurs during AD pathology. Dynamic analyses involving bifurcation diagrams and phase differences demonstrate that the current excitation <i>I</i><sub><i>HR</i></sub> in the HR neuron, which mimics βAP action, disrupts phase synchronization by impairing astrocytic calcium homeostasis and synaptic function. Furthermore, while both chemical and electrical synaptic coupling strengths can modulate synchronization, they ultimately fail to counteract severe pathology. Similarly, astrocyte feedback exhibits compensatory potential only under mild conditions but becomes ineffective under high <i>I</i><sub><i>HR</i></sub> excitation. Collectively, these findings pinpoint key mechanisms behind AD network degeneration and establish a dynamical foundation for therapies targeting neuroinflammation and electrical dysregulation.</p>

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Electrical activity in a memristor synapse-coupled astrocyte-neuronal motif

  • 期刊论文

  • 发表日期：

    2026年4月16日

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  • Fudong Li,
  • Yongjun Gan,
  • Chunlai Li,
  • Peng Su

摘要

Although β-amyloid (Aβ) accumulation is a cardinal pathological hallmark of Alzheimer’s disease (AD), it also critically disrupts synchronized activity in glia-neuronal motifs—an electrophysiological manifestation closely associated with cognitive decline. This dysfunction stems from Aβ-induced neuroinflammation and impaired synaptic plasticity. To investigate this, we present a multi-scale coupled heterogeneous astrocyte-neuronal model that comprises a Hindmarsh-Rose (HR) pyramidal neuron, a Morris-Lecar (ML) interneuron, and an astrocyte to explore the electrical activity within a minimal glia-neuronal motif. This model dynamically simulates, through astrocyte, the positive feedback of endoplasmic reticulum calcium leakage and mitochondrial calcium overload triggered by β-amyloid protein (βAP), while regulates synaptic plasticity in real time through glial neurotransmitter release. Meanwhile, a memristor is employed to model the non-monotonic attenuation of synaptic weights and the resultant imbalance between long-term potentiation (LTP) and long-term depression (LTD) that occurs during AD pathology. Dynamic analyses involving bifurcation diagrams and phase differences demonstrate that the current excitation IHR in the HR neuron, which mimics βAP action, disrupts phase synchronization by impairing astrocytic calcium homeostasis and synaptic function. Furthermore, while both chemical and electrical synaptic coupling strengths can modulate synchronization, they ultimately fail to counteract severe pathology. Similarly, astrocyte feedback exhibits compensatory potential only under mild conditions but becomes ineffective under high IHR excitation. Collectively, these findings pinpoint key mechanisms behind AD network degeneration and establish a dynamical foundation for therapies targeting neuroinflammation and electrical dysregulation.