title: Nicotine leads to improvements in behavioral impairment and an increase in the nicotine acetylcholine receptor in transgenic mice.
abstract: Nicotine is the principal psychoactive ingredient in cigarette smoke, and has been associated with health problems in humans. However, the pure form of nicotine may prove to be a valuable pharmaceutical agent for the treatment of AD. However, the beneficial effects of nicotine remain a matter of much controversy. In order to clarify this issue, 12-month-old transgenic mice, expressing neuron-specific enolase (NSE)-controlled APPsw, were treated with low, middle, and high doses of nicotine for 6 months. Herein, we have concluded that the nicotine-treated groups evidenced improvements in behavior and increases in the nicotine acetylcholine receptor, nAchRalpha7. These findings provide experimental evidence that nicotine effects an improvement in impaired memory, and that this improvement is associated with an increase in nAchRalpha7. Thus, nicotine may prove a good preventative or therapeutic modality for AD patients.
authors.affiliation: Team of Laboratory Animal Resources, National Institute of Toxicological Research, Korea Food and Drug Administration, 194 Tongilro Eunpyung-ku, Seoul, 122-704, Republic of Korea.
authors.forename: Sun B
authors.initials: SB
authors.lastname: Shim
authors.forename: Se H
authors.initials: SH
authors.lastname: Lee
authors.forename: Kab R
authors.initials: KR
authors.lastname: Chae
authors.forename: Chuel K
authors.initials: CK
authors.lastname: Kim
authors.forename: Dae Y
authors.initials: DY
authors.lastname: Hwang
authors.forename: Byoung G
authors.initials: BG
authors.lastname: Kim
authors.forename: Seung W
authors.initials: SW
authors.lastname: Jee
authors.forename: Su H
authors.initials: SH
authors.lastname: Lee
authors.forename: Ji S
authors.initials: JS
authors.lastname: Sin
authors.forename: Chang J
authors.initials: CJ
authors.lastname: Bae
authors.forename: Byoung C
authors.initials: BC
authors.lastname: Lee
authors.forename: Hyung H
authors.initials: HH
authors.lastname: Lee
authors.forename: Yong K
authors.initials: YK
authors.lastname: Kim
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D005260:Female; D006801:Humans; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D051379:Mice; D008822:Mice, Transgenic; D015394:Molecular Structure; D009538:Nicotine / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D018722:Nicotinic Agonists / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D010751:Phosphopyruvate Hydratase / Q000235:genetics; D011978:Receptors, Nicotinic / Q000378:metabolism*; D064569:alpha7 Nicotinic Acetylcholine Receptor
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; C579167:Chrna7 protein, human; C579166:Chrna7 protein, mouse; D018722:Nicotinic Agonists; D011978:Receptors, Nicotinic; D064569:alpha7 Nicotinic Acetylcholine Receptor; D009538:Nicotine; D010751:Phosphopyruvate Hydratase