In vivo axonal transport rates decrease in a mouse model of Alzheimer's disease

Neuroimage. 2007 May 1;35(4):1401-8. doi: 10.1016/j.neuroimage.2007.01.046. Epub 2007 Feb 12.

Abstract

Axonopathy is a pronounced attribute of many neurodegenerative diseases. In Alzheimer's disease (AD), axonal swellings and degeneration are prevalent and may contribute to the symptoms of AD senile dementia. Current limitations in identifying the contribution of axonal damage to AD include the inability to detect when this damage occurs in relation to other identifiers of AD because of the invasiveness of existing methods. To overcome this, we further developed the MRI methodology Manganese Enhanced MRI (MEMRI) to assess in vivo axonal transport rates. Prior to amyloid-beta (Abeta) deposition, the axonal transport rates in the Tg2576 mouse model of AD were normal. As Abeta levels increased and before plaque formation, we observed a significant decrease in axonal transport rates of the Tg2576 mice compared to controls. After plaque formation, the decline in the transport rate in the Tg2576 mice became even more pronounced. These data indicate that in vivo axonal transport rates decrease prior to plaque formation in the Tg2576 mouse model of AD.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / pathology
  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / genetics
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Axonal Transport / physiology*
  • Blotting, Western
  • Body Temperature / physiology
  • Colchicine / pharmacology
  • Data Interpretation, Statistical
  • Kinetics
  • Magnetic Resonance Imaging
  • Manganese / pharmacology
  • Mice
  • Mice, Inbred C57BL
  • Plaque, Amyloid / metabolism
  • Plaque, Amyloid / pathology

Substances

  • Amyloid beta-Peptides
  • Manganese
  • Colchicine