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Progressive neuronal loss and dysfunction characterize neurodegenerative diseases (NDs) such as Alzheimer's, Parkinson's, and Huntington's diseases, spinal cord injury, and stroke, making them difficult to treat. Curcumin, a bioactive substance derived from the turmeric plant (Curcuma longa), is interesting due to its potential neuroprotective properties. This review thoroughly shows the cellular and molecular signaling mechanisms that curcumin utilizes to provide neuroprotective effects in NDs. Curcumin regulates several signaling pathways linked to neuroprotection, such as those that reduce oxidative stress, prevent Aβ formation, and decrease neuroinflammation. NF-κB suppression reduces inflammatory responses, while Nrf2 activation boosts antioxidant response element expression. Furthermore, curcumin enhances autophagy and neurotrophic factor expression, facilitating the removal of harmful protein aggregates. The function of curcumin as a metal chelator is emphasized particularly to iron and other metal dysregulations linked to neurodegenerative processes. Curcumin's capacity to regulate metal ion homeostasis is essential since the pathophysiology of NDs is significantly influenced by metal-induced oxidative stress and toxic buildup. It shows potential therapeutic effects by reducing oxidative damage and chelating excess metals. Clinical research indicates that curcumin can penetrate the blood-brain barrier, making it an effective treatment option. The regulation of these pathways reduces neuronal damage and improves neurons' survival and functionality. In addition, curcumin's anti-inflammatory properties and low toxicity make it a promising long-term treatment option for NDs. Therefore, this review emphasizes the potential of curcumin as a targeted neuroprotective compound, presenting recent clinical insights and experimental data. Future studies should optimize curcumin formulations and delivery systems to enhance its bioavailability and therapeutic efficacy.
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http://dx.doi.org/10.1002/jbt.70369 | DOI Listing |
Inflammopharmacology
September 2025
Centre for Research Impact & Outcome, Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India.
The NOD‑like receptor family pyrin domain containing 3 (NLRP3) inflammasome is a key molecular complex that amplifies inflammatory cascades by maturing interleukin‑1 beta (IL-1β) and interleukin‑18 (IL-18) and inducing pyroptosis. It serves as a major driver and co-driver of numerous diseases associated with chronic inflammation. Dysregulated NLRP3 activation contributes to the progression of disorders such as rheumatoid arthritis, inflammatory bowel disease, neurodegenerative diseases and atherosclerosis.
View Article and Find Full Text PDFCell Biochem Biophys
September 2025
Faculty of Industrial Sciences and Technology, Universiti Malaysia Pahang Al-Sultan Abdullah, Lebuhraya Persiaran Tun Khalil Yaakob, Gambang, Kuantan, Pahang, Malaysia.
J Drug Target
September 2025
Department of Pharmacology, Rajarshi Shahu College of Pharmacy, Buldana, Maharashtra, INDIA.
Natural phytoconstituents such as betanin and curcumin have attracted interest for their significant antioxidant and anti-inflammatory properties. Their therapeutic efficacy is notably constrained by inadequate bioavailability and reduced skin permeability. The current study developed an ethosome-based gel system for the delivery of betanin and curcumin, with the objective of improving transdermal penetration and providing sustained anti-inflammatory effects.
View Article and Find Full Text PDFFood Sci Nutr
September 2025
Department of Nutrition Sciences, School of Health Larestan University of Medical Sciences Iran.
Chronic myeloid leukemia (CML), a myeloproliferative neoplasm, is characterized by the fusion gene, which results in constitutive tyrosine kinase activity. While tyrosine kinase inhibitors (TKIs) have significantly improved CML outcomes, resistance and the persistence of leukemic stem cells remain major clinical challenges. Curcumin, a natural polyphenol derived from , has demonstrated potential anticancer properties.
View Article and Find Full Text PDFVet World
July 2025
Department of Basic Medical Sciences, Division of Physiology, Manipal Academy of Higher Education, Manipal, Karnataka, India.
Arsenic exposure remains a critical global health concern, with growing evidence linking it to significant kidney dysfunction. This review examines the underlying mechanisms of arsenic-induced nephrotoxicity, including oxidative stress, mitochondrial dysfunction, inflammation, and programmed cell death, which collectively contribute to damage in the glomeruli and renal tubules. Chronic exposure is associated with proteinuria, renal impairment, and an increased risk of chronic kidney disease (CKD).
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