Background: Chronic ethanol (EtOH) consumption results in a variety of central nervous system (CNS) deficits, including behavioral alteration and cognitive deficiencies like learning and memory problems. The current investigation aims to evaluate malvidins ability to protect rats memories from EtOH-induced impairments. Methods: A total of 24 male Wistar rats were randomly selected and allotted into 4 groups (n = 6): Group-I served as control and received saline solution (1 mL/kg p.o.), Group-II-EtOH control (2 mg/kg, i.p.) and Group-III and IV were treated with malvidin (lower-100 and higher-200 mg/kg dose p.o.) along with EtOH (2 mg/kg, i.p.) for 45 days. The efficacy of malvidin at higher and lower doses was evaluated using an experimentally induced EtOH-induced memory deficit model in rats. Spatial and working memory performance was assessed using the Y-maze and Morris water maze (MWM) tests. Biochemical markers were analyzed, including choline acetyltransferase (ChAT), acetylcholinesterase (AChE), glutathione (GSH), superoxide dismutase (SOD), nitrate, catalase (CAT), and malonaldehyde (MDA) levels. A ferric reducing/antioxidant power (FRAP) assay assessed antioxidant capacity. Glutamate (Glu) and gamma-aminobutyric acid (GABA) levels were measured to evaluate neurotransmitter function. Pro-inflammatory cytokine levels, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and IL-6, were quantified to assess neuroinflammatory responses. Caspase-3 activity was measured as an apoptosis marker. Additionally, molecular docking simulations were performed to investigate potential interactions between malvidin and relevant molecular targets. Results: Malvidin at both dosage levels, demonstrated a significant (p < 0.001) attenuated EtOH-induced memory impairments in rats. That was evident through improved performance in Y-maze and MWM tests. Malvidin treatment at both concentrations substantially (p < 0.001) restored ChAT and antioxidant levels (GSH, SOD, CAT, and FRAP). Additionally, malvidin significantly (p < 0.001) reduced AChE levels, MDA levels, neuroinflammatory markers (IL-1β, TNF-α, and IL-6), and the apoptosis marker (caspase-3) when compared to the EtOH control group. Molecular docking studies suggested a potential interaction between malvidin and relevant targets involved in memory function and neuroinflammation. Malvidin had a favorable affinity towards glutamate, AChE, and ChAT with docking scores of –9.754, –9.329 and –8.234 kcal/mol. Conclusion: The findings of this study indicate that malvidin, especially at higher doses, exerts neuroprotective effects against EtOH-induced memory impairments in rats. The observed improvements in memory function may be associated with the restoration of cholinergic activity, oxidative stress modulation, neuroinflammation suppression, and potential interactions with crucial molecular targets. These findings hold significant promise for the advancement of novel neuroprotective therapeutics.