Mangiferin, a polyphenol of natural occurrence predominantly present in Mangifera indica, has attracted significant interest because of its multiplicity of pharmacological activities, of which its neuroprotective activity is of particular interest. Herein, the review delves into the biosynthetic mechanisms, structural properties, and action mechanisms responsible for the therapeutic value of mangiferin in neurological disorders. Of special note is that mangiferin has antioxidative, anti-inflammatory, and anti-apoptotic activities, which are responsible for its effectiveness in reducing cognitive impairments and neuronal damage in disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, stroke, epilepsy, depression, anxiety, and general cognitive decline. Though being of low bioavailability, more recent approaches such as chemical derivatization, nanoparticle-mediated drug delivery, and intranasal delivery have the promise to enhance its central nervous system (CNS) delivery. By combining preclinical and mechanistic studies, the review herein highlights the potential of mangiferin as a multitherapeutic neuroprotectant and addresses new approaches to facilitate its clinical application.

Purpurin (1,2,4-trihydroxy-9,10-anthraquinone) is a naturally occurring anthraquinone pigment derived primarily from Rubia species. Beyond its traditional use as a natural dye, purpurin has recently gained attention for its multifaceted pharmacological activities, particularly in neuroprotection. This review outlines the biosynthetic pathways leading to anthraquinone formation via the shikimate, mevalonate, and methylerythritol phosphate routes, culminating in the generation of purpurin. Structure–activity relationship analyses highlight the critical role of hydroxyl substitutions in modulating antioxidant, anticancer, antibacterial, and neuroprotective properties through radical stabilization, DNA intercalation, and metal chelation. Evidence from preclinical studies indicates that purpurin exerts beneficial effects in Alzheimer’s disease, depression, ischemic stroke, and age-related cognitive decline, primarily through anti-tau aggregation, cholinesterase inhibition, serotonergic modulation, antioxidant activity, and anti-inflammatory mechanisms. While purpurin exhibits low acute toxicity and promising pharmacodynamics, its therapeutic translation remains limited by poor solubility, rapid metabolism, and low brain bioavailability. Nanotechnology-based formulations and molecular modifications are being explored to overcome these challenges. Collectively, purpurin represents a versatile bioactive scaffold with considerable potential for the development of multifunctional neuroprotective agents.

Folic Acid (FA) is introducing itself as a useful addition to wound management protocol. Herein, we report a novel eco-friendly method to prepare silver nanoparticles (AgNPs) using the anabolic FA as a reducing agent.