Aluminium neurotoxicity is implicated in Alzheimer's disease, which is marked by progressive memory loss, cognitive impairment and structural degeneration, leading to complete incapacitation. Formation of excess reactive oxygen species causes oxidative stress, which is the hallmark of aluminium toxicity. A quest to counteract these pathologies led to investigating Zingiber officinale (ZO) extracts on cognitive and anti-oxidative potentials against aluminium chloride (AlCl3)-induced neurotoxicity in Swiss mice. The oral lethal dose of ZO was estimated as 4,743 mg/kg. Forty-eight adult female Swiss mice of weight 21-27 g were then assigned to eight groups (n=6): Group 1 were the control (40 mL/kg distilled water), while groups 2-8 were respectively, administered AlCl3 (100 mg/kg) alone, and with Donepezil (2.5 mg/kg), ZO ethanol extract (474, 949 and 1,423 mg/kg), ZO dichloromethane (949 mg/kg), and ZO methanol (949 mg/kg) extracts for 21 days. The classic labyrinth test was carried out subsequently, the animals sacrificed, and their brain homogenized for biochemical assay. There was a significantly (p<0.05) increased latency to complete the labyrinth test by the AlCl3 group compared with the control. The ZO extracts treated groups had decreased latency to complete the labyrinth test, and these were significant (p<0.05) in the 949 and 1,423 mg/kg ethanol extract groups. Biochemically, AlCl3 significantly (p<0.05) elevated acetyl cholinesterase and malondialdehyde levels, while reducing superoxide dismutase activity: These adverse effects were reversed significantly (p<0.05) following treatment with extracts of ZO. In conclusion, ZO ethanol extract and its dichloromethane and methanol fractions improved cognitive activities, and possessed anticholinesterase, anti-oxidant and neuroprotective potentials.