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<p>Metabolic synergy between astrocytes and neurons is key to maintaining normal brain function. As the main supporting cells in the brain, astrocytes work closely with neurons through intercellular metabolic synergy networks to jointly regulate energy metabolism, lipid metabolism, synaptic transmission, and cerebral blood flow. This important synergy is often disrupted in neurological diseases such as Alzheimer’s disease, Parkinson’s disease, and stroke. This study systematically explores the physiological basis of this intercellular collaboration and its dysfunctional manifestations in the aforementioned diseases, and provides detailed insights into how abnormalities in specific collaborative pathways (such as impaired lactate transport, disrupted glutamate cycling, or lipid processing defects) significantly contribute to disease progression. By elucidating the molecular mechanisms underlying these collaborative impairments, this study aims to identify potential therapeutic targets, with the core strategy being to restore these critical intercellular collaborative relationships to alleviate neurological diseases.</p>

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Astrocyte-Neuron Metabolic Synergies in Neurological Homeostasis and Disease

  • 期刊论文

  • 发表日期：

    2025年9月9日

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  • Jiahao Dong,
  • Zihan Gao,
  • Mingrui Liu,
  • Binglu Qian,
  • Cheng Yuan,
  • Hui Liu,
  • Ni Rao,
  • Yingjiao Liu

摘要

Metabolic synergy between astrocytes and neurons is key to maintaining normal brain function. As the main supporting cells in the brain, astrocytes work closely with neurons through intercellular metabolic synergy networks to jointly regulate energy metabolism, lipid metabolism, synaptic transmission, and cerebral blood flow. This important synergy is often disrupted in neurological diseases such as Alzheimer’s disease, Parkinson’s disease, and stroke. This study systematically explores the physiological basis of this intercellular collaboration and its dysfunctional manifestations in the aforementioned diseases, and provides detailed insights into how abnormalities in specific collaborative pathways (such as impaired lactate transport, disrupted glutamate cycling, or lipid processing defects) significantly contribute to disease progression. By elucidating the molecular mechanisms underlying these collaborative impairments, this study aims to identify potential therapeutic targets, with the core strategy being to restore these critical intercellular collaborative relationships to alleviate neurological diseases.