Curcumin is the primary curcuminoid present in the Curcuma longa rhizome, commonly
known as turmeric, and because of its potential as a natural anticancer drug, it has drawn a lot of scientific
attention. Curcumin has a broad range of pharmacological activities, such as antioxidant, antiinflammatory,
antimicrobial, antiangiogenic, anticancer, antiproliferative, and many more. Curcumin
has been demonstrated in numerous in vitro and in vivo investigations to be capable of preventing the
development and spread of a number of malignancies, including those of the breast, colon, prostate,
lung, stomach, brain, and pancreas. Curcumin’s capacity to alter a broad spectrum of molecular targets
implicated in tumor initiation, development, and progression is thought to be the cause of its anticancer
properties. These include the control of tumor suppressor genes, apoptotic proteins, inflammatory
mediators, and angiogenic factors, as well as important signaling pathways like NF-κB, PI3K/
Akt, Wnt/β-catenin, and MAPK. Although curcumin has a potential pharmacological profile, its therapeutic
effectiveness is severely limited by its low bioavailability. Numerous formulation techniques,
such as the use of adjuvants (such as piperine), liposomes, nanoparticles, and micelles, have shown
promising results in improving systemic availability and therapeutic potency. This study demonstrates
the complex role curcumin plays in the fight against cancer and stresses how crucial it is to get
past pharmacokinetic obstacles in order to fully utilise its therapeutic potential. Curcumin shows
promise as an efficient, low-toxicity drug in integrative cancer therapy with additional study and clinical
validation. This review provides an integrated cross-cancer analysis of curcumin-mediated signaling
networks and translational strategies to overcome pharmacokinetic limitations.
K. Sannidhi, Navya, A. M. Ashesh et al.· Current Cancer Therapy Revie...· 0 citations
The Alzheimer's Disease (AD) lacks effective disease-modifying therapy, even though amyloid-targeting immunotherapies have recently been applied clinically. N-methyl-D-Aspartate Receptors (NMDARs) play a central yet mechanistically complicated role in the pathophysiology of AD, where they are convergence points of amyloid-beta (Aβ) oligomer toxicity, tau-dependent excitotoxicity, and progressive synaptic failure. This critical review examines NMDAR dysfunction across the AD spectrum, with a focus on subunit-regulated signalling, subcellular localisation, and subsequent pathological cascades. The effects of Aβ oligomers on NMDAR activity involve multiple mechanisms that disrupt their function, including glutamate dysregulation mediated by GLT-1, redistribution of GluN2B to extrasynaptic areas, and inhibition of JAK2-CREB via activation of extrasynaptic receptors. Tau enhances excitotoxic injury throughdendritic mislocalization, and the tau-Fyn-GluN2B complex, which propels pro-death signalling by DAPK1. This conceptually important prevailing synaptic-extrasynaptic dichotomy is fiercely criticised here, given evidence that synaptic receptors containing GluN2A also mediate pathological signalling during sustained Aß exposure, and that tri-heteromeric receptor populations are problematic for subunit-selective targeting. Neuroinflammation, dysfunction of the blood-brain barrier, and excitotoxic amplification via GluN2C/D-enriched receptor pools in neurons, astrocytes, microglia, oligodendrocytes, and endothelial cells are underexplored therapeutic targets for neurodegenerative disease (non-neuronal NMDARs). Memantine is the only approved NMDAR-targeting agent for AD. Subunit-selective antagonists have not been translated into clinical use, and the positive allosteric modulator dalzanemdor (SAGE-718) did not pass its randomised Phase 2 trial in 2024. The most mechanistically justified approach is to advance subunit-selective, compartment-specific, or protein-complexdisrupting strategies. Although it is not established whether any single NMDAR-targeting intervention will suffice as a disease-modifying therapy, the convergence of molecular, genetic, and clinical evidence positions NMDAR dysfunction as a tractable , if therapeutically demanding , node in the AD pathogenic network, warranting continued, mechanism-informed drug discovery.
Md Sirajuddin Khan, A. M. Ashesh, Mithul V. Mammen et al.· Current Neuropharmacology· 0 citations
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