title: Ferulic acid reverses the cognitive dysfunction caused by amyloid β peptide 1-40 through anti-oxidant activity and cholinergic activation in rats.
abstract: Cholinergic dysfunction and oxidation stress are the dominant mechanisms of memory deficit in Alzheimer's disease (AD). This study describes how ferulic acid (FA) ameliorates cognitive deficits induced by mecamylamine (MECA), scopolamine (SCOP), central acetylcholinergic neurotoxin ethylcholine mustard aziridinium ion (AF64A) and amyloid β peptide (Aβ1-40). This study also elucidates the role of anti-oxidant enzymes and cholinergic marker acetylcholinesterase (AChE) in the reversal of FA from Aβ1-40-induced cognitive deficits in rats. At 100 mg/kg, FA attenuated impairment induced by MECA and SCOP plus MECA; however, this improvement was not blocked by the peripheral muscarinic receptor antagonist scopolamine methylbromide (M-SCOP). At 100 and 300 mg/kg, FA also attenuated the impairment of inhibitory passive avoidance induced by AF64A. Further, FA attenuated the performance impairment and memory deficit induced by Aβ1-40 in rats, as did vitamin E/C. FA reversed the deterioration of superoxide dismutase (SOD) and AChE activities, and the glutathione disulfide (GSSG) and glutathione (GSH) levels in the cortex and hippocampus. Vitamin E/C only selectively reversed deterioration in the hippocampus. We suggest that FA reduced the progression of cognitive deficits by activating central muscarinic and nicotinic receptors and anti-oxidant enzymes.
authors: School of Chinese Medicines for Post-Baccalaureate, I-Shou University, Kaohsiung 82445, Taiwan.
authors: Fan-Shiu
authors: FS
authors: Tsai
authors: Lung-Yuan
authors: LY
authors: Wu
authors: Shu-Er
authors: SE
authors: Yang
authors: Hao-Yuan
authors: HY
authors: Cheng
authors: Chin-Chuan
authors: CC
authors: Tsai
authors: Chi-Rei
authors: CR
authors: Wu
authors: Li-Wei
authors: LW
authors: Lin
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D000975:Antioxidants; D002540:Cerebral Cortex / Q000378:metabolism; D018678:Cholinergic Agents; D003072:Cognition Disorders / Q000188:drug therapy* / Q000209:etiology* / Q000517:prevention & control; D003373:Coumaric Acids / Q000494:pharmacology* / Q000627:therapeutic use*; D004195:Disease Models, Animal; D006624:Hippocampus / Q000378:metabolism; D007858:Learning / Q000187:drug effects; D008297:Male; D010446:Peptide Fragments / Q000378:metabolism*; D017207:Rats, Sprague-Dawley; D011976:Receptors, Muscarinic / Q000378:metabolism; D011978:Receptors, Nicotinic / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D000975:Antioxidants; D018678:Cholinergic Agents; D003373:Coumaric Acids; D010446:Peptide Fragments; D011976:Receptors, Muscarinic; D011978:Receptors, Nicotinic; C078592:amyloid beta-protein (1-40); C004999:ferulic acid; D013482:Superoxide Dismutase; D000110:Acetylcholinesterase
keywords: AF64A; Aβ1-40; Ferulic Acid; Learning Paradigms; Rats