ArticleActa neuropathologica communications2016
Revisiting rodent models: Octodon degus as Alzheimer's disease model?
Article in Acta neuropathologica communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- Age-Associated Behavioral Alterations in Laboratory-Housed Octodon degus.bioRxiv : the preprint server for biology · 2026Article
- The central cholinergic system as a therapeutic target in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Untargeted plasma metabolomics in canine cognitive dysfunction: the naturally occurring Alzheimer's disease analog in dogs.Frontiers in neuroscience · 2026Article
- Article
- Diabetic retinopathy and Alzheimer's disease: Convergence of the unfolded protein response in neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Beyond Transgenic Mice: Emerging Models and Translational Strategies in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Exploring efficient and effective mammalian models for Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- Lost in translation: Inconvenient truths on the utility of mouse models in Alzheimer's disease research.eLife · 2024Review
- Alzheimer's Disease Neuropathological Change in Aged Non-Primate Mammals.International journal of molecular sciences · 2024Review
- Article
- Alzheimer's Disease: Models and Molecular Mechanisms Informing Disease and Treatments.Bioengineering (Basel, Switzerland) · 2024Review
- In-silico structural analysis ofMolecular biology research communications · 2024Article
- Review
- Physiological expression of mutated TAU impaired astrocyte activity and exacerbates β-amyloid pathology in 5xFAD mice.Journal of neuroinflammation · 2023Article
- Zn-dependent β-amyloid Aggregation and its Reversal by the Tetrapeptide HAEE.Aging and disease · 2023Article
- Time- and Sex-Dependent Effects of Fingolimod Treatment in a Mouse Model of Alzheimer's Disease.Biomolecules · 2023Article
- Cognitively impaired aged Octodon degus recapitulate major neuropathological features of sporadic Alzheimer's disease.Acta neuropathologica communications · 2022Article
- A Novel Huntington's Disease Assessment Platform to Support Future Drug Discovery and Development.International journal of molecular sciences · 2022Article
- Bridging the Gap: A Geroscience Primer for Neuroscientists With Potential Collaborative Applications.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.