Purpose: Alzheimer's is a disease affecting mostly the Older population leading to the deterioration of cognitive capabilities. The protective effect of Caffeic acid in Colchicineinduced dementia was evaluated in the current study. Materials and Methods: Colchicine was administered intracerebroventricularly (ICV) to the lateral ventricle of the brain (at the coordinates 0.8 mm posterior to bregma, 1.8 mm lateral to the sagittal suture, 3.6 mm below the cortical surface) using robotic stereotaxic apparatus that results in Alzheimer's type sporadic dementia. Caffeic acid at the dose of 50 mg/kg p.o, was administered daily for 25 days starting four days before the colchicine injection and evaluated for its neuroprotective activity. The spatial memory of animals was evaluated using Morris water maze followed by biochemical estimations of acetylcholinesterase and antioxidant markers in the hippocampal and frontal cortex region of the brain. Results: Intracerebroventricular injection of colchicine in rat brain resulted in decreased cognitive abilities as evident in escape latency and average speed of the retention trial. Significant changes in the escape latency were noted in Caffeic acid-treated group. The level of acetylcholinesterase and antioxidant markers like glutathione, catalase, lipid peroxidation, superoxide dismutase were significantly changed in the hippocampal region of the rats but not in the frontal cortex region in the caffeic acid treatment groups. Conclusion: The current study provides evidence for the neuroprotective and antioxidative potential of caffeic acid in intracerebroventricularly injected Colchicine-induced sporadic model of AD.

bleaching process, gets converted to sesamol readily. 3 PHYSICOCHEMICAL PROPERTIES OF SESAMOL Sesamol is found as crystalline needles with pale brown color in nature with a peculiar odor. Sesamol's melting point was observed to be 64°C ± 1°C with no signs of hygroscopicity, while the solubility was found to be 38.8 ± 1.2 mg/ml in water at 37°C. Sesamol shows solubility of approximately 10 mg/ml at all the pH <9 and a sharp increase in solubility with more alkaline pH >10 and the value being 41.83 mg/ml at pH 13. The ionization constant (pKa) value of sesamol is 9.79 ± 0.06. The predicted and experimental log P values for sesamol are 1.29 ± 0.01 and 1.34, respectively. Distribution coefficient (log D), of sesamol and the value, is found to vary in the range of 1.0-2.0, though the pH-solubility profile of sesamol was found to be persistent between pH 1.0 and 7.0. 4

Background: Dementia is a neurodegenerative disorder majorly evidenced by cognitive impairment. Although there are many types of dementia, the common underlying etiological factors in all the types are neuro-inflammation or ageing induced apoptosis. β-caryophyllene, a cannabinoid type-2 receptor agonist has reported to have promising neuroprotective effects in cerebral ischemia and neuro-inflammation. Objective: In the present study, we evaluated the effects of β-caryophyllene, against animal models of dementia whose etiology mimicked neuro-inflammation and ageing. Method: Two doses (50 and 100 mg/kg of body weight) of β-caryophyllene given orally were tested against AlCl3-induced dementia in male Sprague Dawley (SD) rats using Morris water maze test. Subsequently, the effect of the drug was assessed for episodic memory in female SD rats using novel object recognition task in doxorubicin-induced neuro-inflammation and male SD rats for chemobrain model. Moreover, its effects were evaluated in D-galactose-induced mitochondrial dysfunction leading to dementia. Results: β-caryophyllene, at both the doses, showed significant improvement in memory when assessed using parameters like target quadrant entries, escape latency and path efficiency in Morris water maze test for spatial memory. In the doxorubicin-induced chemobrain model, β-caryophyllene at 100 mg/kg significantly elevated acetylcholinesterase and catalase levels and lowered lipid peroxidation compared to the disease control. In the novel object recognition task, β-caryophyllene at 100 mg/kg significantly improved recognition index and discrimination index in the treated animals compared to the disease control, with a significant increase in catalase and decrease in lipid peroxidation in both hippocampus and frontal cortex. However, in D-galactose-induced mitochondrial dysfunction model, β-caryophyllene failed to show positive effects when spatial memory was assessed. It also failed to improve D-galactose induced diminished mitochondrial complex I and II activities. Conclusion: Hence, we conclude that β-caryophyllene at 100 mg/kg protects against dementia induced by neuro-inflammation with no effect on neuronal aging induced by mitochondrial dysfunction.