Interplay Between Oxidative Stress, Autophagy and the Endocannabinoid System in Neurodegenerative Diseases: Role of the Nrf2- p62/SQSTM1 Pathway and Nutraceutical Activation DOI Open Access
Federica Armeli, Beatrice Mengoni, Debra L. Laskin

et al.

Published: June 6, 2024

The onset of neurodegenerative diseases involves a complex interplay pathological mecha-nisms, including protein aggregation, oxidative stress, impaired autophagy. This review focuses on the intricate connection between stress and autophagy in disor-ders, highlighting as pivotal disease pathogenesis. Reactive oxygen species (ROS) play dual roles cellular homeostasis regulation, with disruptions redox sig-naling contributing to neurodegeneration. activation Nrf2 pathway represents criti-cal antioxidant mechanism, while maintains by degrading al-tered cell components. interaction p62/SQSTM1, Keap1 forms regulatory essential for response, whose dysregulation leads aggregate accumulation. Targeting Nrf2-p62/SQSTM1 holds promise thera-peutic intervention, mitigating preserving functions. Additionally, explores potential synergy endocannabinoid system signal-ing neuroprotection. Further research is needed elucidate involved molecular mecha-nisms develop effective therapeutic strategies against

Language: Английский

Interplay Between Oxidative Stress, Autophagy and the Endocannabinoid System in Neurodegenerative Diseases: Role of the Nrf2- p62/SQSTM1 Pathway and Nutraceutical Activation DOI Open Access
Federica Armeli, Beatrice Mengoni, Debra L. Laskin

et al.

Published: June 6, 2024

The onset of neurodegenerative diseases involves a complex interplay pathological mecha-nisms, including protein aggregation, oxidative stress, impaired autophagy. This review focuses on the intricate connection between stress and autophagy in disor-ders, highlighting as pivotal disease pathogenesis. Reactive oxygen species (ROS) play dual roles cellular homeostasis regulation, with disruptions redox sig-naling contributing to neurodegeneration. activation Nrf2 pathway represents criti-cal antioxidant mechanism, while maintains by degrading al-tered cell components. interaction p62/SQSTM1, Keap1 forms regulatory essential for response, whose dysregulation leads aggregate accumulation. Targeting Nrf2-p62/SQSTM1 holds promise thera-peutic intervention, mitigating preserving functions. Additionally, explores potential synergy endocannabinoid system signal-ing neuroprotection. Further research is needed elucidate involved molecular mecha-nisms develop effective therapeutic strategies against

Language: Английский

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