*p*<0.05, statistically different from cisplatin-treated group.

**5. Biochemical evidences** 

**5.1 Cholinergic relationship with Sch B** 

medicated nerve transmission. (Tabet 2006).

**Entries in open arms**

**B**

**cDDP**

Fig. 4. Effect of Sch B (10, 25, and 50 mg/kg) on the EPM task against cisplatin. (A) Total number of entries (B) Entries in open arms. Data are represented as the mean S.E.M (n=8).

For a quarter of a century, the pathogenesis of AD associated dementia has been linked to a deficiency in the brain neurotransmitter acetylcholine (ACh). This was based on the observations of cholinergic system abnormalities leading to intellectual impairment. Subsequently, the 'cholinergic hypothesis' of AD gained considerable acceptance. It stated that a serious loss of cholinergic function in the central nervous system contributed to cognitive symptoms. Over the years, both evidence for and challenges to the relationship between ACh dysfunction and AD have been put forward, and acetylcholinesterase inhibitors (AChEIs) were introduced for the symptomatic treatment of AD. The prevailing view is that the efficacy of AChEIs is attained through their augmentation of ACh-

**SchB10+cDDP**

**SchB25+cDDP**

**SchB50+cDDP**
