TY - JOUR
T1 - Natural AD-like neuropathology in octodon degus
T2 - Impaired burrowing and neuroinflammation
AU - Deacon, Robert M.J.
AU - Altimiras, Francisco J.
AU - Bazán-León, Enrique A.
AU - Pyarasani, Rhada D.
AU - Nachtigall, Fabiane M.
AU - Santos, Leonardo S.
AU - Tsolaki, Anthony G.
AU - Pednekar, Lina
AU - Kishore, Uday
AU - Biekofsky, Rodolfo R.
AU - Vásquez, Rodrigo A.
AU - Cogram, Patricia
N1 - Publisher Copyright:
© 2015 Bentham Science Publishers.
PY - 2015/5/1
Y1 - 2015/5/1
N2 - 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.
AB - 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.
KW - Alzheimer’s disease
KW - Beta-amyloid
KW - Burrowing
KW - Complement
KW - Cytokines
KW - Octodon degus
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UR - http://www.scopus.com/inward/citedby.url?scp=84929611667&partnerID=8YFLogxK
U2 - 10.2174/1567205012666150324181652
DO - 10.2174/1567205012666150324181652
M3 - Article
C2 - 25817252
AN - SCOPUS:84929611667
SN - 1567-2050
VL - 12
SP - 314
EP - 322
JO - Current Alzheimer Research
JF - Current Alzheimer Research
IS - 4
ER -
