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A-mediated synaptic glutamate dynamics and calcium dynamics in astrocytes associated with Alzheimer's disease. | LitMetric

A-mediated synaptic glutamate dynamics and calcium dynamics in astrocytes associated with Alzheimer's disease.

Cogn Neurodyn

School of Mathematics and Statistics, Shaanxi Normal University, Xi'an, 710119 People's Republic of China.

Published: December 2024

AI Article Synopsis

  • The accumulation of amyloid peptides is believed to significantly contribute to the development of Alzheimer's disease by targeting astrocytes and disrupting glutamate signaling.
  • A mathematical model was created to analyze how various pathways (GLT-syn, GLT-ess, mGluR, NMDAR, Glio-Rel) influenced synaptic and extrasynaptic glutamate levels as well as intracellular calcium signaling in astrocytes.
  • Findings indicated that GLT-syn was the most critical pathway for affecting synaptic glutamate, while GLT-ess and Glio-Rel impacted extrasynaptic glutamate, with potential implications for therapeutic strategies to mitigate cell death from glutamate dysregulation in Alzheimer’s disease.

Article Abstract

The accumulation of amyloid peptide is assumed to be one of the main causes of Alzheimer's disease . There is increasing evidence that astrocytes are the primary targets of A. A can cause abnormal synaptic glutamate, aberrant extrasynaptic glutamate, and astrocytic calcium dysregulation through astrocyte glutamate transporters facing the synaptic cleft (GLT-syn), astrocyte glutamate transporters facing the extrasynaptic space (GLT-ess), metabotropic glutamate receptors in astrocytes (mGluR), N-methyl-D-aspartate receptors in astrocytes (NMDAR), and glutamatergic gliotransmitter release (Glio-Rel). However, it is difficult to experimentally identify the extent to which each pathway affects synaptic glutamate, extrasynaptic glutamate, and astrocytic calcium signaling. Motivated by these findings, this work established a concise mathematical model of astrocyte dynamics, including the above A-mediated glutamate-related multiple pathways. The model results presented the extent to which five mechanisms acted upon by A affect synaptic glutamate, extrasynaptic glutamate, and astrocytic intracellular signals. We found that GLT-syn is the main pathway through which A affects synaptic glutamate. GLT-ess and Glio-Rel are the main pathways through which A affects extrasynaptic glutamate. GLT-syn, mGluR, and NMDAR are the main pathways through which A affects astrocytic intracellular signals. Additionally, we discovered a strong, monotonically increasing relationship between the mean glutamate concentration and the mean oscillation amplitude (or frequency). Our results may have therapeutic implications for slowing cell death induced by the combination of glutamate imbalance and dysregulation in AD.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655814PMC
http://dx.doi.org/10.1007/s11571-024-10064-6DOI Listing

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