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Acta Neuropathol Commun. 2016 Aug 26;4(1):91. doi: 10.1186/s40478-016-0363-y.

Revisiting rodent models: Octodon degus as Alzheimer's disease model?

Author information

1
University of Lübeck (UzL), LIED, Lübeck, Germany.
2
Department of Neuro-/Pathology, University of Oslo (UiO) & Oslo University Hospital (OUS), Oslo, Norway.
3
Leibniz Institute for Plant Biochemistry (IPB), Halle, Germany.
4
Department of Neuropathology, Heinrich Heine University Düsseldorf (HHU), Düsseldorf, Germany.
5
Department of Zoology/Developmental Neurobiology, Otto von Guericke University Magdeburg (OvGU), Magdeburg, Germany.
6
University of Lübeck (UzL), LIED, Lübeck, Germany. jens.pahnke@medisin.uio.no.
7
Department of Neuro-/Pathology, University of Oslo (UiO) & Oslo University Hospital (OUS), Oslo, Norway. jens.pahnke@medisin.uio.no.
8
Leibniz Institute for Plant Biochemistry (IPB), Halle, Germany. jens.pahnke@medisin.uio.no.
9
Department of Pathology (PAT), Translational Neurodegeneration Research and Neuropathology Lab, University of Oslo, Postboks 4950, Nydalen, 0424, Oslo, Norway. jens.pahnke@medisin.uio.no.

Abstract

Alzheimer's disease primarily occurs as sporadic disease and is accompanied with vast socio-economic problems. The mandatory basic research relies on robust and reliable disease models to overcome increasing incidence and emerging social challenges. Rodent models are most efficient, versatile, and predominantly used in research. However, only highly artificial and mostly genetically modified models are available. As these 'engineered' models reproduce only isolated features, researchers demand more suitable models of sporadic neurodegenerative diseases. One very promising animal model was the South American rodent Octodon degus, which was repeatedly described as natural 'sporadic Alzheimer's disease model' with 'Alzheimer's disease-like neuropathology'. To unveil advantages over the 'artificial' mouse models, we re-evaluated the age-dependent, neurohistological changes in young and aged Octodon degus (1 to 5-years-old) bred in a wild-type colony in Germany. In our hands, extensive neuropathological analyses of young and aged animals revealed normal age-related cortical changes without obvious signs for extensive degeneration as seen in patients with dementia. Neither significant neuronal loss nor enhanced microglial activation were observed in aged animals. Silver impregnation methods, conventional, and immunohistological stains as well as biochemical fractionations revealed neither amyloid accumulation nor tangle formation. Phosphoepitope-specific antibodies against tau species displayed similar intraneuronal reactivity in both, young and aged Octodon degus.In contrast to previous results, our study suggests that Octodon degus born and bred in captivity do not inevitably develop cortical amyloidosis, tangle formation or neuronal loss as seen in Alzheimer's disease patients or transgenic disease models.

KEYWORDS:

Alzheimer’s disease; Amyloid beta-Peptides; Animal models; Neurodegenerative diseases; Neuropathology; Octodon degus; Rodentia; Tau proteins

PMID:
27566602
PMCID:
PMC5002178
DOI:
10.1186/s40478-016-0363-y
[Indexed for MEDLINE]
Free PMC Article

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