Lack of spontaneous age-related brain pathology in Octodon degus: a reappraisal of the model.

Mathieu Bourdenx, Sandra Dovero, Marie-Laure Thiolat, Erwan Bezard, Benjamin Dehay
Sci Rep. 2017-04-04; 7(1):
DOI: 10.1038/srep45831

PubMed
Lire sur PubMed



1. Sci Rep. 2017 Apr 4;7:45831. doi: 10.1038/srep45831.

Lack of spontaneous age-related brain pathology in Octodon degus: a reappraisal
of the model.

Bourdenx M(1)(2), Dovero S(1)(2), Thiolat ML(1)(2), Bezard E(1)(2), Dehay
B(1)(2).

Author information:
(1)Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000
Bordeaux, France.
(2)CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux,
France.

Neurodegenerative diseases are characterized by the degeneration of specific
brain areas associated with accumulation of disease-related protein in extra- or
intra-cellular deposits. Their preclinical investigations are mostly based on
genetically-engineered animals. Despite their interest, these models are often
based on high level of disease-related protein expression, thus questioning their
relevance to human pathology and calling for the alternate use of ecological
models. In the past few years, Octodon degus has emerged as a promising animal
model displaying age-dependent Alzheimer’s disease-related pathology. As
neurodegenerative-related proteins often co-deposit in the brain of patients, we
assessed the occurrence of α-synuclein-related pathology in this model using
state-of-the-art immunohistochemistry and biochemistry. Despite our efforts and
in contrast with previously published results, our study argues against the use
of Octodon degus as a suitable natural model of neurodegenerative disorder as we
failed to identify either Parkinson’s disease- or Alzheimer’s disease-related
brain pathologies.

DOI: 10.1038/srep45831
PMCID: PMC5379186
PMID: 28374864

Auteurs Bordeaux Neurocampus