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<p>Neurodegenerative diseases are characterized by progressive neuronal dysfunction and loss, resulting from dysregulation of multiple programmed cell death pathways, including autophagy, apoptosis, and necroptosis. Growing evidence suggests that oxidative stress and inflammatory cues promote extensive cross-talk among these processes, leading to dynamic switching between cell survival and death. This review focuses on the coordinated regulation of autophagy, apoptosis, and necroptosis, particularly the emerging role of key molecular mediators such as DAPK1, RIPK1, Beclin‑1, MLKL, ULK1, UVRAG, and cGAS-STING in shaping neuronal fate across neurodegenerative conditions. Dysregulated DAPK1 activity has been linked to protein aggregation and activation of apoptotic and necrotic pathways, contributing to neuronal loss in neurodegenerative diseases. In parallel, RIPK1 acts as a&#xa0;key determinant of cell fate decisions downstream of inflammatory signaling, while autophagy-associated regulators such as ULK1, Beclin‑1, and UVRAG influence the balance between protective and detrimental outcomes. In addition, cGAS-STING activation can trigger inflammatory cell death (pyroptosis), which worsens neuron damage in neurodegenerative diseases. Overall, this review highlights the importance of maintaining a&#xa0;finely tuned balance among autophagy, apoptosis, and necroptosis in neurodegenerative diseases. Understanding the functional interplay among these pathways may provide valuable insights into therapeutic strategies to limit neuronal loss and disease progression. The literature cited was retrieved through a&#xa0;comprehensive search of major scientific databases, including PubMed, Scopus, ScienceDirect, and Web of Science.</p>

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Signaling cross-talk driving neuronal survival, death and inflammation in neurodegeneration

  • 期刊论文

  • 发表日期：

    2026年4月21日

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  • Lovedeep Singh

摘要

Neurodegenerative diseases are characterized by progressive neuronal dysfunction and loss, resulting from dysregulation of multiple programmed cell death pathways, including autophagy, apoptosis, and necroptosis. Growing evidence suggests that oxidative stress and inflammatory cues promote extensive cross-talk among these processes, leading to dynamic switching between cell survival and death. This review focuses on the coordinated regulation of autophagy, apoptosis, and necroptosis, particularly the emerging role of key molecular mediators such as DAPK1, RIPK1, Beclin‑1, MLKL, ULK1, UVRAG, and cGAS-STING in shaping neuronal fate across neurodegenerative conditions. Dysregulated DAPK1 activity has been linked to protein aggregation and activation of apoptotic and necrotic pathways, contributing to neuronal loss in neurodegenerative diseases. In parallel, RIPK1 acts as a key determinant of cell fate decisions downstream of inflammatory signaling, while autophagy-associated regulators such as ULK1, Beclin‑1, and UVRAG influence the balance between protective and detrimental outcomes. In addition, cGAS-STING activation can trigger inflammatory cell death (pyroptosis), which worsens neuron damage in neurodegenerative diseases. Overall, this review highlights the importance of maintaining a finely tuned balance among autophagy, apoptosis, and necroptosis in neurodegenerative diseases. Understanding the functional interplay among these pathways may provide valuable insights into therapeutic strategies to limit neuronal loss and disease progression. The literature cited was retrieved through a comprehensive search of major scientific databases, including PubMed, Scopus, ScienceDirect, and Web of Science.