Targeting protein kinase C signaling cascades in alzheimer's disease: emerging neuroprotective roles of aurothioglucose.

Protein Kinase C (PKC), a zinc-dependent signaling enzyme pivotal for neuronal survival and synaptic plasticity, has emerged as a central player in the pathogenesis of Alzheimer's disease (AD). Dysregulated PKC activity contributes to amyloid-β accumulation, tau-driven neurofibrillary tangles, and chronic neuroinflammation, mediated through key molecular cascades such as NF-κB, GSK-3β, and MAPK. Notably, conditions such as osteoporosis and rheumatoid arthritis further illustrate how chronic cytokine release can link systemic inflammation to PKC dysregulation and subsequent neurodegeneration. Although mechanistic insights into these pathways have expanded, AD remains a therapeutic enigma with no disease-modifying interventions available. Interestingly, traditional Indian medical texts like the Charaka-Samhita documented herbal and metallic remedies, including gold-based formulations such as Swarna Prashana, reputed for enhancing cognition. Translating this ancient wisdom into modern medicine, aurothioglucose, an FDA-approved agent for rheumatoid arthritis, has demonstrated potent anti-inflammatory properties through PKC modulation. Emerging preclinical evidence now positions aurothioglucose as a promising neuroprotective candidate, capable of mitigating oxidative stress, dampening neuroinflammation, and preserving synaptic integrity via PKC-linked pathways. This review underscores the evolving role of aurothioglucose in AD, highlighting its potential to bridge traditional knowledge with contemporary therapeutics, while emphasizing the pressing need for translational studies to confirm its disease-modifying efficacy, as supported by evidences from current state of art.