Potential Utilization of Natural Anthraquinone Aglycone Emodin for Alzheimer's Disease: A Comprehensive Review With Computational Insights

Emodin (EMO), a naturally occurring anthraquinone aglycone, has attracted considerable attention for its potential therapeutic application against Alzheimer's disease (AD). This study presents a comprehensive review integrated with molecular docking and ADMET‐based computational analyses to investigate the anti‐Alzheimer's potential of EMO. A systematic evaluation of published literature was conducted alongside in silico pharmacokinetic, toxicity, and target‐binding assessments to explore its multitarget neuroprotective properties. The findings indicate that EMO modulates several AD‐related pathological pathways, including oxidative stress, neuroinflammation, amyloid‐beta aggregation, cholinergic dysfunction, and neuronal cytotoxicity. Molecular docking demonstrated strong binding affinities toward major AD‐associated targets, including acetylcholinesterase, Nrf2, and JNK1, with binding energies of −9.7, −9.7, and −9.3 kcal/mol, respectively, suggesting stable molecular interactions. Pharmacokinetic predictions revealed favorable oral bioavailability, acceptable drug‐likeness, and moderate gastrointestinal absorption, although limited blood–brain barrier permeability was observed. Toxicity profiling suggested an overall acceptable safety profile despite possible mutagenic and nephrotoxic effects. Collectively, these findings support EMO as a promising multitarget therapeutic candidate for AD, warranting further experimental and clinical validation. Additionally, EMO exhibited favorable interaction patterns compared with co‐crystal ligands, highlighting its therapeutic relevance in neurodegenerative disorders. Nevertheless, the absence of in vivo studies and human clinical evidence remains a major limitation requiring future investigation.