Abstract
Alzheimer’s disease (AD) is the most common cause of dementia, affecting more than 36 million people worldwide. Octodon degus, a South American rodent, has been found to spontaneously develop neuropathological signs of AD, including amyloid-β (Aβ) and tau deposits, as well as a decline in cognition with age. Firstly, the present work introduces a novel behavioral assessment for O. degus - the burrowing test - which appears to be a useful tool for detecting neurodegeneration in the O. degus model for AD. Such characterization has potentially wide-ranging implications, because many of these changes in species-typical behaviors are reminiscent of the impairments in activities of daily living (ADL), so characteristic of human AD. Furthermore, the present work characterizes the ADlike neuropathology in O. degus from a gene expression point of view, revealing a number of previously unreported AD biomarkers, which are found in human AD: amyloid precursor protein (APP), apolipoprotein E (ApoE), oxidative stressrelated genes from the NFE2L2 and PPAR pathway, as well as pro-inflammatory cytokines and complement proteins, in agreement with the known link between neurodegeneration and neuroinflammation. In summary, the present results confirm a natural neuropathology in O. degus with similar characteristics to AD at behavioral, cellular and molecular levels. These characteristics put O. degus in a singular position as a natural rodent model for research into AD pathogenesis and therapeutics against AD.
Keywords: Alzheimer’s disease, beta-amyloid, burrowing, complement, cytokines, Octodon degus.
Current Alzheimer Research
Title:Natural AD-Like Neuropathology in Octodon degus: Impaired Burrowing and Neuroinflammation
Volume: 12 Issue: 4
Author(s): Robert M.J. Deacon, Francisco J. Altimiras, Enrique A. Bazan-Leon, Rhada D. Pyarasani, Fabiane M. Nachtigall, Leonardo S. Santos, Anthony G. Tsolaki, Lina Pednekar, Uday Kishore, Rodolfo R. Biekofsky, Rodrigo A. Vasquez and Patricia Cogram
Affiliation:
Keywords: Alzheimer’s disease, beta-amyloid, burrowing, complement, cytokines, Octodon degus.
Abstract: Alzheimer’s disease (AD) is the most common cause of dementia, affecting more than 36 million people worldwide. Octodon degus, a South American rodent, has been found to spontaneously develop neuropathological signs of AD, including amyloid-β (Aβ) and tau deposits, as well as a decline in cognition with age. Firstly, the present work introduces a novel behavioral assessment for O. degus - the burrowing test - which appears to be a useful tool for detecting neurodegeneration in the O. degus model for AD. Such characterization has potentially wide-ranging implications, because many of these changes in species-typical behaviors are reminiscent of the impairments in activities of daily living (ADL), so characteristic of human AD. Furthermore, the present work characterizes the ADlike neuropathology in O. degus from a gene expression point of view, revealing a number of previously unreported AD biomarkers, which are found in human AD: amyloid precursor protein (APP), apolipoprotein E (ApoE), oxidative stressrelated genes from the NFE2L2 and PPAR pathway, as well as pro-inflammatory cytokines and complement proteins, in agreement with the known link between neurodegeneration and neuroinflammation. In summary, the present results confirm a natural neuropathology in O. degus with similar characteristics to AD at behavioral, cellular and molecular levels. These characteristics put O. degus in a singular position as a natural rodent model for research into AD pathogenesis and therapeutics against AD.
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Cite this article as:
Deacon M.J. Robert, Altimiras J. Francisco, Bazan-Leon A. Enrique, Pyarasani D. Rhada, Nachtigall M. Fabiane, Santos S. Leonardo, Tsolaki G. Anthony, Pednekar Lina, Kishore Uday, Biekofsky R. Rodolfo, Vasquez A. Rodrigo and Cogram Patricia, Natural AD-Like Neuropathology in Octodon degus: Impaired Burrowing and Neuroinflammation, Current Alzheimer Research 2015; 12 (4) . https://dx.doi.org/10.2174/1567205012666150324181652
DOI https://dx.doi.org/10.2174/1567205012666150324181652 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |

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