This study aimed to investigate the effect of induced dementia due to low dose of aluminum chloride (AlCl3) in rotenone model of Parkinson's disease. Male mice were treated for two weeks with one of the following: AlCl3 (2 mg/kg, i.p.); rotenone (1.5 mg/kg, s.c.); AlCl3 + rotenone; vehicle. Behavioral tests as: rearing activity, wire hanging, stair tests and Morris water maze (WMZ) together with histopathological examinations were done. The brain malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO), paraoxonase-1 (PON-1) and butyrylcholinesterase were also determined. Results indicated that administration of AlCl3, rotenone or their combination caused elevation in brain MDA and nitric oxide and decreased GSH content. Cortical PON-1 activity decreased by AlCl3 or rotenone and showed more decrease after AlCl3/rotenone co-treatment. Butyrylcholinesterase activity in cortex decreased by rotenone, but increased after AlCl3 and AlCl3/rotenone co-treatment. Both AlCl3 and rotenone impaired performance in WMZ, wire hanging and stair tests and decreased rearing behavior. AlCl3/rotenone co-treatment resulted in higher impairment in behavioral tests compared with that caused by either AlCl3 or rotenone. These data indicate that oxidative stress is involved in neurotoxicity caused by either AlCl3 or rotenone; AlCl3 administration didn't enhance oxidative stress and neurodegeneration caused by rotenone although a low dose of AlCl3 worsened rotenone-induced motor and memory impairment. Increased intake of this metal therefore is likely to worsen motor and cognitive symptoms in idiopathic Parkinson's disease (PD).