Therapeutic potential of sulforaphane in neurodegenerative diseases: mechanistic Insights into Nrf2, NF-κB, TrkB, SIRT1, MAPK, and JAK/STAT signalling pathways.
Therapeutic potential of sulforaphane in neurodegenerative diseases: mechanistic Insights into Nrf2, NF-κB, TrkB, SIRT1, MAPK, and JAK/STAT signalling pathways.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Patna, IN · Author affiliation
Department of Pharmacology, Bihar College of Pharmacy, New Bailey Road, Patna, 801503, Bihar, India. omkar.official.955@gmail.com.Location evidence
Amritsar, IN · Author affiliation
Department of Pharmaceutical Sciences, Guru Nanak Dev University, 143005, Punjab, Amritsar, India.Location evidence
Haridwar, IN · Author affiliation
Motherhood University, Roorkee-Dehradun Road, Haridwar, Uttarakhand, 247661, India.Location evidence
Jaipur, IN · Author affiliation
Amity Institute of Pharmacy, Amity University, Jaipur, Rajasthan, India.Location evidence
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Original abstract
Neurodegenerative diseases, including Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis, are chronic and progressive disorders distinguished by neuronal dysfunction, oxidative stress, neuroinflammation, and abnormal protein aggregation. Due to the multifactorial nature of these disorders, current pharmacotherapies provide limited symptomatic relief without altering disease progression. Sulforaphane, a naturally occurring isothiocyanate abundant in cruciferous vegetables like broccoli, has emerged as a potent neuroprotective compound owing to its pleiotropic effects on key cellular signalling pathways. This review provides a thorough overview of the mechanistic insights underlying SFN’s neuroprotective potential, with a focus on the modulation of key signalling pathways such as Nrf2/ARE, NFĸB, BDNF/TrkB, SIRT1, MAPK, and JAK/STAT. Through the activation of antioxidant defenses and suppression of inflammatory cascades, SFN effectively mitigates neuronal damage and supports cellular homeostasis. Preclinical studies consistently demonstrate SFN’s ability to attenuate oxidative stress, inhibit apoptosis, preserve mitochondrial function, and improve neurobehavioral outcomes. While limited clinical evidence supports its safety and bioactivity, further investigations are needed to establish its therapeutic utility in human populations. Overall, SFN represents a promising natural compound with significant potential for the prevention and management of neurodegenerative diseases through multi-targeted pathway modulation.