Biogerontology

, Volume 7, Issue 1, pp 43–52

Elevated Oxidative Stress in the Brain of Senescence-accelerated Mice at 5 Months of Age

  • Óscar Álvarez-García
  • Ignacio Vega-Naredo
  • Verónica Sierra
  • Beatriz Caballero
  • Cristina Tomás-Zapico
  • Antonio Camins
  • José Joaquín García
  • Mercè Pallàs
  • Ana Coto-Montes
Research article

DOI: 10.1007/s10522-005-6041-2

Cite this article as:
Álvarez-García, Ó., Vega-Naredo, I., Sierra, V. et al. Biogerontology (2006) 7: 43. doi:10.1007/s10522-005-6041-2

Abstract

The senescence-accelerated mouse (SAM) is a useful animal model to study aging or age-associated disorder. In the present study, we have used a multidisciplinary approach to the characterization of changes that occur in aging and in the modelling of brain aging. The SAMP8 mouse at 5 months of age exhibited an increase in gliosis and molecular oxidative damage. Likewise, we found that superoxide dismutase activity decreased compared with age-matched SAMR1 while there were no differences in activity of catalase and glutathione reductase. These results indicate that the decrease of superoxide dismutase may be involved in the increase of oxidative stress in brain of SAMP8 at younger stages. This suggestion is supported by an increase in the expression of alpha-synuclein together with phosphorylated tau protein, which is concurrent with the decline of that antioxidant enzyme. Alpha-synuclein aggregates are invariably associated with tau pathologies and our results demonstrate that alpha-synuclein accumulation is a potent inducer of tau pathologies not only in neurodegenerative diseases but also in normal aging. These results also imply that SAMP8 are exposed to elevated levels of oxidative stress from an early age, and that could be a very important cause of the senescence-related impairments and degeneration in the brain seen in this strain.

Keywords

agingalpha-synucleinantioxidant defencebrain damagegliosisoxidative stresssenescence-accelerated model mouse (SAM)tau phosphorylation

Abbreviations

4HDA

4-hydroxyalkenal

AD

Alzheimer’s disease

AS

alpha-Synuclein

CAT

catalase

GR

glutathione reductase

LB

Lewy Bodies

LPO

lipid peroxidation

MDA

malondialdehyde

PD

protein damage

PHF

paired helicoidal filament

ROS

reactive oxygen species

SAM

senescence-accelerated mouse

SOD

superoxide dismutase

Copyright information

© Springer 2006

Authors and Affiliations

  • Óscar Álvarez-García
    • 1
  • Ignacio Vega-Naredo
    • 1
  • Verónica Sierra
    • 1
  • Beatriz Caballero
    • 1
  • Cristina Tomás-Zapico
    • 1
  • Antonio Camins
    • 2
  • José Joaquín García
    • 3
  • Mercè Pallàs
    • 2
  • Ana Coto-Montes
    • 1
  1. 1.Department of Morphology and Cellular Biology, Faculty of MedicineUniversity of OviedoOviedoSpain
  2. 2.Department of Pharmacology, Faculty of PharmacyUniversity of BarcelonaBarcelonaSpain
  3. 3.Department of Pharmacology and Physiology, Faculty of MedicineUniversity of ZaragozaSpain