## 2.1 Introduction  
The scopolamine-induced memory impairment model is the most widely used pharmacological model for anti-dementia drug screening. The anti-muscular receptor drug scopolamine efficiently causes memory disruption by blocking the cholinergic nerve system [1, 2, 3]. Models of amnesia have been established using scopolamine; mice or rats can be utilized with dosages ranging from 0.5 mg/kg to 5 mg/kg for single/or multiple doses [4]. Repeated doses of scopolamine have been shown to cause more impairment in memory function in the passive avoidance test than a single dose of scopolamine [5].  
The role of oxidative damage in human diseases, such as neurodegenerative disorders (NDs), and changes in the activity of the antioxidant and/or other enzymes in the organisms, has become an increasingly important research field for NDs. Scopolamine is known to increase the production of endogenous reactive oxygen species and pro-inflammatory cytokines leading to severe nervous system damage, especially in the hippocampus and/or prefrontal cortex regions [2, 6, 7]. In oxidative stress conditions, brain neurotransmitters with acetylcholine (Ach) and monoamine neurotransmitters are likely inactivated. Lipidperoxidation yields malondialdehydedehyde (MDA) and antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) are thought to be crucial in combating oxidative stress [8; 9; 10; 11; 12]. Although many enzymes related to oxidative stress in NDs have been studied, Paraoxonase (PON), Carbonic Anhydrase (CA), and \(\beta\)-glucosidase enzymes are within the scope of our study. The PON enzyme family has a well-established role in the prevention of cardiovascular disease and demonstrates anti-inflammatory and antioxidant capabilities. Additionally, they have been connected to the beginning and development of numerous neurological conditions and neurodegenerative diseases [13; 14; 15]. \(\beta\)-glucosidase plays important roles in a variety of crucial physiological processes, particularly cytosolic \(\beta\)-glucosidase, which demonstrates important activity towards many common dietary xenobiotics including drugs, although the question regarding the impact of scopolamine on liver and serum cytosolic \(\beta\)-glucosidase in mammals has not been answered yet [16; 17]. CA dysfunction affects cognition and is linked to mental retardation, Alzheimer's disease, and aging according to an increasing body of research [18]. Patients with Carbonic anhydrase II (CAII) deficiencies exhibit cognitive impairments that range in severity from mild deficits to severe mental retardation [19; 20]. In the hippocampal of Alzheimer's disease (AD) patients, an increase in oxidized proteins has been also reported, including CAII [21; 22].  
The fact that approximately 152 million people--three times the present estimate of 50 million--are predicted to suffer dementia by 2050 serves as a stark reminder of the significance of neurodegenerative diseases [23]. Therefore, this study aimed to evaluate CA activity changes from erythrocytes with PON and \(\beta\)-glucosidase level changes in serum and liver tissues of young, adult, and middle-aged rats and scopolamine-induced memory impairment rats.