ORIGINAL ARTICLE Curcumin improves episodic memory in cadmium induced memory impairment through inhibition of acetylcholinesterase and adenosine deaminase activities in a rat model Ayodele Jacob Akinyemi 1 & Princess Kamsy Okonkwo 1 & Opeyemi Ayodeji Faboya 2,3 & Sunday Amos Onikanni 1 & Adewale Fadaka 1 & Israel Olayide 1 & Elizabeth Olufisayo Akinyemi 4 & Ganiyu Oboh 5 Received: 7 June 2016 /Accepted: 28 July 2016 # Springer Science+Business Media New York 2016 Abstract Curcumin, the main polyphenolic component of tur- meric (Curcuma longa) rhizomes has been reported to exert cognitive enhancing potential with limited scientific basis. Hence, this study sought to evaluate the effect of curcumin on cerebral cortex acetylcholinesterase (AChE) and adenosine de- aminase (ADA) activities in cadmium (Cd)-induced memory impairment in rats. Animals were divided into six groups (n = 6): saline/vehicle, saline/curcumin 12.5 mg/kg, saline/ curcumin 25 mg/kg, Cd/vehicle, Cd/curcumin 12.5 mg/kg, and Cd/curcumin 25 mg/kg. Rats received Cd (2.5 mg/kg) and curcumin (12.5 and 25 mg/kg, respectively) by gavage for 7 days. The results of this study revealed that cerebral cortex AChE and ADA activities were increased in Cd-poisoned rats, and curcumin co-treatment reversed these activities to the control levels. Furthermore, Cd intoxication in- creased the level of lipid peroxidation in cerebral cortex with a concomitant decreased in functional sulfuhydryl (-SH) group and nitric oxide (NO), a potent neurotransmitter and neuromodulatory agent. However, the co-treatment with curcumin at 12.5 and 25 mg/kg, respectively increased the non-enzymatic antioxidant status and NO in cerebral cortex with a decreased in malondialdehyde (MDA) level. Therefore, inhibition of AChE and ADA activities as well as increased antioxidant status by curcumin in Cd-induced memory dys- function could suggest some possible mechanism of action for their cognitive enhancing properties. Keywords Curcumin . Cadmium . Cerebral cortex . Acetylcholinesterase . Adenosine deaminase Introduction Cadmium (Cd) is a noxious environmental contaminant of con- tinuing great toxicological concern worldwide (Johri et al. 2010). It is a highly accumulative toxicant with very long bio- logical half-life of over 20 years (Johri et al. 2010). It has been reported that Cd can enter into the food chain since it is not degraded in the environment and this is one of the main route of exposure in humans (Olsson et al. 2002). In this way, the prolonged exposure to Cd has been linked to toxic effects trig- gered by the accumulation of this metal in a variety of structures of the central nervous system (CNS) (Sinha et al. 2009). Studies have shown that Cd is able to cross the blood–brain barrier (BBB) and accumulate in the brain (Sinha et al. 2009) leading to cerebral edema, impairment of attention, learning and memory as well an increase in aggressive and anxiogenic-like behaviors and also worsening of the synaptic neurotransmission and the antioxidant levels (Mendez-Armenta et al. 2001, 2003; Goncalves et al. 2010; Abdalla et al. 2014). In addition, Cd can cause changes in key enzymes of the CNS involved in main- taining the levels of important neurotransmitter and neuropro- tective agent (Goncalves et al. 2010, 2012; Abdalla et al. 2014). * Ayodele Jacob Akinyemi ajakinyemi2010@yahoo.co.uk 1 Department of Chemical Science, Biochemistry Unit, Afe Babalola University Ado-Ekiti, Private Mail Bag 5454, Nigeria 2 Department of Medicine, Ekiti State University Ado-Ekiti, Private Mail Bag 5363, Nigeria 3 Department of Clinical Science, Ekiti State University Teaching Hospital, Ado-Ekiti, Nigeria 4 Center for Child and Adolescence Mental Health (CCAMH), College of Medicine, University of Ibadan, Ibadan, Nigeria 5 Department of Biochemistry, Federal University of Technology, Akure, Ondo State, Nigeria Metab Brain Dis DOI 10.1007/s11011-016-9887-x