Neurodegenerative diseases represent a growing global challenge linked to aging, sharing core pathogenic mechanisms such as oxidative stress, neuroinflammation, and mitochondrial decay. This review evaluates the neuroprotective potential of specific polyphenols and carotenoids in modulating key signaling pathways. These nutraceuticals promote the nuclear translocation of Nrf2, the master regulator of antioxidant defenses, while simultaneously inhibiting the NF-κB pathway to suppress pro-inflammatory cytokine production. By facilitating the microglial switch from neurotoxic to neuroprotective phenotype, these bioactive compounds effectively break the cycle of chronic neuronal damage. While these molecules offer a promising non-invasive strategy to delay disease progression, significant gaps remain regarding their bioavailability and blood-brain barrier crossing. Future research must prioritize clinical trials to translate these molecular insights into effective nutritional interventions, highlighting the necessity of precision nutraceutical protocols in modern neurology.
Resveratrol, Curcumin, and Carotenoids in Nrf2 Activation: Molecular Mechanisms and Potential Role for the Treatment of Neurodegenerative Diseases / Armeli, F., Mengoni, B., Crudeli, M.L., Menin, M., Businaro, R.. - In: BIOCELL. - ISSN 1667-5746. - 0:0(2026), pp. 1-10. [10.32604/biocell.2026.084039]
Resveratrol, Curcumin, and Carotenoids in Nrf2 Activation: Molecular Mechanisms and Potential Role for the Treatment of Neurodegenerative Diseases
Armeli, Federica
Primo
;Mengoni, Beatrice;Crudeli, Maria Luisa;Menin, Martina;Businaro, Rita
2026
Abstract
Neurodegenerative diseases represent a growing global challenge linked to aging, sharing core pathogenic mechanisms such as oxidative stress, neuroinflammation, and mitochondrial decay. This review evaluates the neuroprotective potential of specific polyphenols and carotenoids in modulating key signaling pathways. These nutraceuticals promote the nuclear translocation of Nrf2, the master regulator of antioxidant defenses, while simultaneously inhibiting the NF-κB pathway to suppress pro-inflammatory cytokine production. By facilitating the microglial switch from neurotoxic to neuroprotective phenotype, these bioactive compounds effectively break the cycle of chronic neuronal damage. While these molecules offer a promising non-invasive strategy to delay disease progression, significant gaps remain regarding their bioavailability and blood-brain barrier crossing. Future research must prioritize clinical trials to translate these molecular insights into effective nutritional interventions, highlighting the necessity of precision nutraceutical protocols in modern neurology.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


