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Updated: Apr 18, 2026

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
Published on: March 22, 2016
Accelerating Alzheimer's research through 'natural' animal models
Nady Braidy1, Anne Poljak, Tharusha Jayasena
1aCentre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales bSchool of Medical Sciences, University of New South Wales cBioanalytical Mass Spectrophotometry Facility, University of New South Wales, Sydney, New South Wales, Australia dFaculty of Biological Sciences, Centre for Ageing and Regeneration (CARE), P. Catholic University of Chile, Santiago, Republic of Chile eNeuropsychiatric Institute, Prince of Wales Hospital, Sydney, New South Wales, Australia.
Naturally aged animal models, like rats, dogs, and Octodon degus, show Alzheimer's disease-like symptoms. These models offer better insights into Alzheimer's disease mechanisms and therapeutic development than transgenic models.
Area of Science:
- Neuroscience
- Gerontology
- Pathology
Background:
- Alzheimer's disease (AD) is a complex, multifactorial neurodegenerative disorder linked to aging.
- Current transgenic animal models often fail to fully replicate the molecular, cellular, and behavioral aspects of human AD.
- There is a need for more representative and ecologically valid models to study AD pathogenesis and test interventions.
Purpose of the Study:
- To evaluate the clinical relevance of 'physiologically' aged rats, dogs, and Octodon degus as natural models for Alzheimer's disease research.
- To explore their utility in elucidating mechanistic aspects of AD and developing therapeutics for age-related cognitive decline.
Main Methods:
- Review of existing literature on cognitive decline and Alzheimer's disease-like pathology in naturally aged animal models.
- Comparative analysis of aged rats, dogs, and Octodon degus against human AD pathology and transgenic models.
Main Results:
- Aged rats, dogs, and O. degus exhibit cognitive decline and develop AD-like symptoms due to natural aging.
- While aged rats show cognitive decline, they lack AD pathology. Aged dogs and non-human primates develop amyloid-beta plaques.
- O. degus uniquely display amyloid-beta deposits, tau pathology, altered cholinergic transmission, and cognitive deficits mirroring human AD.
Conclusions:
- Naturally aged animal models provide a more comprehensive representation of Alzheimer's disease pathophysiology compared to transgenic models.
- These 'natural' models are valuable for understanding AD neurobiology and for developing therapeutic strategies with potential for human clinical translation.
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