Curcumin has been extensively investigated as an anticancer agent, yet its clinical application remains constrained by low bioavailability, incomplete mechanistic understanding, and limited therapeutic optimization. In light of growing resistance to conventional chemotherapies and the demand for safer, multi-targeted agents, this review revisits curcumin with a contemporary lens. We critically evaluate the literature published since 2020, focusing on newly elucidated molecular mechanisms by which curcumin regulates tumor progression, including modulation of oncogenic signaling pathways (Wnt/β-catenin, PI3K/Akt/mTOR, JAK/STAT, and MAPK), induction of ferroptosis, and epigenetic reprogramming. A particular emphasis is placed on recent advances in nanoformulation strategies that enhance curcumin’s pharmacokinetic profile and target-specific delivery. Furthermore, the emerging paradigm of combination therapy is explored, where curcumin acts synergistically with chemotherapeutics and phytochemicals to overcome drug resistance and potentiate anticancer efficacy. This review identifies key knowledge gaps, such as inconsistent clinical translation and the underexplored interplay between nanocurcumin systems and immune modulation, outlining directions for future translational research.

Castration-resistant prostate cancer (CRPC) remains a significant therapeutic challenge due to its resistance to standard androgen deprivation therapy (ADT). The emergence of androgen receptor splice variant 7 (AR-V7) has been implicated in CRPC progression, contributing to treatment resistance. Current treatments, including first-generation chemotherapy, androgen receptor blockers, radiation therapy, immune therapy, and PARP inhibitors, often come with substantial side effects and limited efficacy. Natural compounds, particularly those derived from herbal medicine, have garnered increasing interest as adjunctive therapeutic agents against CRPC. This review explores the role of AR-V7 in CRPC and highlights the promising benefits of natural compounds as complementary treatments to conventional drugs in reducing CRPC and overcoming therapeutic resistance. We delve into the mechanisms of action underlying the anti-CRPC effects of natural compounds, showcasing their potential to enhance therapeutic outcomes while mitigating the side effects associated with conventional therapies. The exploration of natural compounds offers promising avenues for developing novel treatment strategies that enhance therapeutic outcomes and reduce the adverse effects of conventional CRPC therapies. These compounds provide a safer, more effective approach to managing CRPC, representing a significant advancement in improving patient care.

Cognitive disorders, including Alzheimer’s disease, Parkinson’s disease, schizophrenia, depression, and vascular dementia, are associated with dysregulation of neurotransmitter systems, including acetylcholine, dopamine, serotonin, glutamate, and γ-aminobutyric acid (GABA). These disorders are increasingly recognized as multifactorial conditions involving oxidative stress, neuroinflammation, mitochondrial dysfunction, synaptic impairment, blood–brain barrier disruption, metabolic imbalance, and gut–brain axis dysregulation. Current pharmacological therapies may provide symptomatic relief; however, their clinical benefits are often limited and associated with adverse effects. Herbal medicines have gained increasing attention as potential complementary approaches for cognitive support and neuroprotection. Preclinical evidence and emerging clinical studies suggest that herbal bioactive compounds may exert neuroprotective effects through antioxidants, anti-inflammatory, and neurotransmitter-modulating mechanisms. Medicinal herbs such as Bacopa monnieri, Withania somnifera, Ginkgo biloba, Glycyrrhiza glabra, Moringa oleifera, and ginseng have shown potential cognitive benefits in experimental models and selected human studies. Advanced delivery systems, including nanoparticles and phytosomes, may further improve the bioavailability and brain-targeting efficiency of herbal compounds. However, current clinical evidence remains heterogeneous and limited by insufficient standardization, small sample sizes, and short study durations. Further large-scale clinical studies and standardized safety assessments are essential before herbal neurotherapeutics can be widely applied in cognitive and neurological disorders.

The authors would like to make the following correction to their published paper