Nicotine reduces A beta in the brain and cerebral vessels of APPsw mice

Eur J Neurosci. 2004 May;19(10):2703-10. doi: 10.1111/j.0953-816X.2004.03377.x.

Abstract

Ten days treatment with nicotine reduced insoluble amyloid A beta 1-40 and Alpha beta 1-42 peptides by 80% in the cortex of 9-month-old APPsw mice, which is more than that observed in 14.5-month-old mice following nicotine treatment for 5.5 months. A reduction in A beta associated with cerebral vessels was observed in addition to that deposited as parenchymal plaques after 5.5 months treatment. The diminution in A beta peptides observed was not accompanied by changes in brain alpha, beta or gamma secretase-like activities, NGF or BDNF protein expression measured in brain homogenates. A significant increase in sAPP was observed after nicotine treatment of SH-SY5Yneuroblastoma cells that could be blocked by the nicotinic antagonist mecamylamine. Attenuation of elevated [(125)I]-alpha bungarotoxin binding (alpha 7) in APPsw mice was observed after 5.5 months nicotine treatment. Both these observations suggest that the reduction in insoluble A beta by nicotine might be in part mediated via the alpha 7 nicotinic receptor. Further studies are required to identify potential mechanisms of the nicotine's amyloid-reducing effect.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Amyloid Precursor Protein Secretases
  • Amyloid beta-Peptides / analysis
  • Amyloid beta-Peptides / blood
  • Amyloid beta-Peptides / metabolism*
  • Amyloid beta-Protein Precursor / genetics
  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Aspartic Acid Endopeptidases
  • Blood Vessels / drug effects*
  • Blotting, Western / methods
  • Brain / drug effects*
  • Brain / metabolism
  • Brain Chemistry
  • Brain-Derived Neurotrophic Factor / metabolism
  • Bungarotoxins / pharmacokinetics
  • Cell Line, Tumor
  • Cerebral Arteries / drug effects*
  • Cerebral Arteries / metabolism
  • Drug Administration Schedule
  • Embryo, Mammalian
  • Endopeptidases / metabolism
  • Glucose Transporter Type 1
  • Humans
  • Immunohistochemistry / methods
  • Iodine Isotopes / pharmacokinetics
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Monosaccharide Transport Proteins / metabolism
  • Nerve Growth Factor / metabolism
  • Neuroblastoma
  • Nicotine / administration & dosage*
  • Nicotine / pharmacology
  • Peptide Fragments / analysis

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Brain-Derived Neurotrophic Factor
  • Bungarotoxins
  • Glucose Transporter Type 1
  • Iodine Isotopes
  • Monosaccharide Transport Proteins
  • Peptide Fragments
  • SLC2A1 protein, human
  • amyloid beta-protein (1-40)
  • amyloid beta-protein (1-42)
  • Nicotine
  • Nerve Growth Factor
  • Amyloid Precursor Protein Secretases
  • Endopeptidases
  • Aspartic Acid Endopeptidases
  • BACE1 protein, human
  • Bace1 protein, mouse