Age-related evolution of amyloid burden, iron load, and MR relaxation times in a transgenic mouse model of Alzheimer's disease

Nadine El Tannir El Tayara; Benoît Delatour; Camille Le Cudennec; Maryvonne Guégan; Andreas Volk; Marc Dhenain

doi:10.1016/j.nbd.2005.10.013

Age-related evolution of amyloid burden, iron load, and MR relaxation times in a transgenic mouse model of Alzheimer's disease

Neurobiol Dis. 2006 Apr;22(1):199-208. doi: 10.1016/j.nbd.2005.10.013. Epub 2005 Dec 7.

Authors

Nadine El Tannir El Tayara¹, Benoît Delatour, Camille Le Cudennec, Maryvonne Guégan, Andreas Volk, Marc Dhenain

Affiliation

¹ Integrative Imaging Unit, Curie Institute-INSERM, Centre Universitaire, Laboratoire 112, 91405 Orsay Cedex, France.

PMID: 16337798
DOI: 10.1016/j.nbd.2005.10.013

Abstract

T1 and T2 magnetic resonance relaxation times have the potential to provide biomarkers of amyloid-beta deposition that could be helpful to the development of new therapies for Alzheimer's disease. Here, we measured T1 and T2 times as well as plaques and iron loads in APP/PS1 mice, which model brain amyloidosis, and control PS1 mice. Iron was mostly associated with amyloid deposits in APP/PS1 animals, while it was diffuse in the PS1 mice. T1 was negatively correlated with age in most structures in APP/PS1 animals. This may be related to the age-associated myelin loss described in APP/PS1 mice rather than to amyloid deposition. T2 in the subiculum of adult APP/PS1 animals was lower than in PS1 mice, which may be related to the very high amyloid and iron loads in this region. T2 in the subiculum could thus serve as an early marker of the amyloid pathology.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Aging / metabolism*
Aging / pathology
Alzheimer Disease / metabolism*
Alzheimer Disease / pathology
Alzheimer Disease / physiopathology*
Amyloid beta-Peptides / biosynthesis
Amyloid beta-Protein Precursor / genetics
Amyloid beta-Protein Precursor / metabolism
Animals
Biomarkers / analysis
Biomarkers / metabolism
Brain / metabolism*
Brain / pathology
Brain / physiopathology*
Cross-Sectional Studies
Demyelinating Diseases / etiology
Demyelinating Diseases / metabolism
Demyelinating Diseases / physiopathology
Disease Models, Animal
Hippocampus / metabolism
Hippocampus / pathology
Hippocampus / physiopathology
Humans
Iron / metabolism*
Magnetic Resonance Imaging
Membrane Proteins / genetics
Membrane Proteins / metabolism
Mice
Mice, Transgenic
Nerve Fibers, Myelinated / metabolism
Nerve Fibers, Myelinated / pathology
Plaque, Amyloid / genetics
Plaque, Amyloid / metabolism*
Plaque, Amyloid / pathology
Presenilin-1

Substances

Amyloid beta-Peptides
Amyloid beta-Protein Precursor
Biomarkers
Membrane Proteins
PSEN1 protein, human
Presenilin-1
Iron