This study investigated the neuromodulatory potential of zinc against acrylamide-induced cognitive impairment. Acrylamide (AA), a toxic substance commonly found in certain foods such as potato, grains and coffee, is known to cause neurological damage and severe cognitive decline. Twenty (20) male Wistar rats were divided into four groups (n = 5) by random selection. All groups except Control (Group 1) which received 1 mL/kg water daily, were induced with an oral dose of 10 mg/kg of Acrylamide. Acrylamide (AA) (Group 2) was left untreated, while Low Zinc (AA + LZN-Group 3) and High zinc (AA + HZN-Group 4) were orally treated respectively with 10 mg/kg and 30 mg/kg of Zinc for 8 weeks. Zinc treatment mitigated the anxiety-like behavior and spatial and non-spatial memory deficit which are all signs of cognitive impairment observed in the AA group. Zinc reverses the significant decrease in superoxide dismutase (SOD) and catalase, significant increase in malondialdehyde (MDA) and interleukin 1β (IL-1β) caused by AA demonstrating its antioxidant and anti-inflammatory properties. Zinc also demonstrated potency in up-regulating brain-derived neurotrophic factor (BDNF) gene expression and down-regulating acetylcholinesterase (AChE) expression. Zinc treatment at both doses significantly increased the number of dentate gyrus cells. This study demonstrates the ability of zinc to mitigate the cognitive impairment secondary to acrylamide exposure.