title: Attenuation of scopolamine-induced cognitive dysfunction by obovatol.
abstract: Alzheimer's disease (AD) is the most prevalent cause of dementia in the elderly people. The disease is pathologically characterized by extracellular deposition of beta-amyloid peptide (Aβ), cholinergic neurodegeneration and elevation of acetylcholine esterase (AChE) activity in the affected regions. In this study, we investigated the effects of obovatol on memory dysfunction, which was caused by scopolamine. Obovatol (0.2, 0.5 and 1 mg/kg for 7 day) attenuated scopolamine (1 mg/kg, i.p.)-induced amnesia in a dose-dependent manner, as revealed by the Morris water maze test and step-through passive avoidance test. Mechanism studies exhibited that obovatol dose-dependently alleviated scopolamine-induced increase in Aβ generation and β-secretase activity in the cortex and hippocampus. Obovatol also attenuated scopolamine-induced rise in AChE activity in the cortex and hippocampus. Obovatol might rescue scopolamine-mediated impaired learning and memory function by attenuating Aβ accumulation and stabilizing cholinergic neurotransmission, which suggests that the natural compound could be a useful agent for the prevention of the development or progression of AD neurodegeneration.
authors.affiliation: College of Pharmacy, Chungbuk National University, Cheongju 361-763, Korea.
authors.forename: Dong-Young
authors.initials: DY
authors.lastname: Choi
authors.forename: Young-Jung
authors.initials: YJ
authors.lastname: Lee
authors.forename: Sun Young
authors.initials: SY
authors.lastname: Lee
authors.forename: Yoot Mo
authors.initials: YM
authors.lastname: Lee
authors.forename: Hyun Hee
authors.initials: HH
authors.lastname: Lee
authors.forename: Im Seop
authors.initials: IS
authors.lastname: Choi
authors.forename: Ki-Wan
authors.initials: KW
authors.lastname: Oh
authors.forename: Sang Bae
authors.initials: SB
authors.lastname: Han
authors.forename: Sang-Yoon
authors.initials: SY
authors.lastname: Nam
authors.forename: Jin Tae
authors.initials: JT
authors.lastname: Hong
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000647:Amnesia / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control* / Q000523:psychology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D002540:Cerebral Cortex / Q000187:drug effects / Q000201:enzymology; D003071:Cognition / Q000187:drug effects*; D003072:Cognition Disorders / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control* / Q000523:psychology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D058851:GPI-Linked Proteins / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology; D008297:Male; D008568:Memory / Q000187:drug effects*; D051379:Mice; D008813:Mice, Inbred ICR; D009043:Motor Activity / Q000187:drug effects; D018697:Nootropic Agents / Q000494:pharmacology*; D010647:Phenyl Ethers / Q000494:pharmacology*; D012601:Scopolamine; D013997:Time Factors
chemical_list: D016229:Amyloid beta-Peptides; D058851:GPI-Linked Proteins; D018697:Nootropic Agents; D010647:Phenyl Ethers; C036796:obovatal; D012601:Scopolamine; D000110:Acetylcholinesterase; C548245:Ache protein, mouse