D-galactose-induced Cognitive Impairment: Mechanism, Models and Therapeutic Interventions

Age is the main risk factor for cognitive impairment, a degenerative disorder marked by deficiencies in memory, learning, and executive function. Although natural ageing research necessitates longer timeframes, animal models are crucial for comprehending causes and creating therapies. Rapid mechanistic study and treatment screening are made possible by the D-galactoseinduced ageing model, induces age-like cognitive and metabolic characteristics in few weeks. A comprehensive literature search was conducted using major scientific databases, including ScienceDirect and Google Scholar. The D-galactose model's current understanding is summarised in this thorough study, which also covers therapeutic approaches, comparative comparison with other ageing models, and molecular pathways. Exposure to D-galactose sets off a series of pathogenic processes that culminate in neuronal malfunction and cognitive impairment. These processes include oxidative stress, advanced glycation end-product (AGE) production, NF-κB and MAPKmediated inflammation, endoplasmic reticulum stress, and apoptosis. With the benefits of quick induction and repeatable outcomes, the model replicates many characteristics of normal ageing, such as cognitive impairments, oxidative damage, and neuroinflammation. Antioxidants (taurine, thymoquinone), anti-inflammatory substances (shikonin, osthole), anti-glycation products, ER stress modulators, and multi-target therapies are among the many therapeutic approaches that have shown promise in the D-galactose model. The model is useful for quick screening and mechanistic hypothesis testing, but further models and clinical research are needed for translational validation.