Hurley, MJ;
Deacon, RMJ;
Beyer, K;
Ioannou, E;
Ibanez, A;
Teeling, JL;
Cogram, P;
(2018)
The long-lived Octodon degus as a rodent drug discovery model for Alzheimer's and other age-related diseases.
Pharmacology & Therapeutics
, 188
pp. 36-44.
10.1016/j.pharmthera.2018.03.001.
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Abstract
Alzheimer's disease (AD) is a multifactorial progressive neurodegenerative disease. Despite decades of research, no disease modifying therapy is available and a change of research objectives and/or development of novel research tools may be required. Much AD research has been based on experimental models using animals with a short lifespan that have been extensively genetically manipulated and do not represent the full spectrum of late-onset AD, which make up the majority of cases. The aetiology of AD is heterogeneous and involves multiple factors associated with the late-onset of the disease like disturbances in brain insulin, oxidative stress, neuroinflammation, metabolic syndrome, retinal degeneration and sleep disturbances which are all progressive abnormalities that could account for many molecular, biochemical and histopathological lesions found in brain from patients dying from AD. This review is based on the long-lived rodent Octodon degus (degu) which is a small diurnal rodent native to South America that can spontaneously develop cognitive decline with concomitant phospho-tau, β-amyloid pathology and neuroinflammation in brain. In addition, the degu can also develop several other conditions like type 2 diabetes, macular and retinal degeneration and atherosclerosis, conditions that are often associated with aging and are often comorbid with AD. Long-lived animals like the degu may provide a more realistic model to study late onset AD.
Type: | Article |
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Title: | The long-lived Octodon degus as a rodent drug discovery model for Alzheimer's and other age-related diseases |
Open access status: | An open access version is available from UCL Discovery |
DOI: | 10.1016/j.pharmthera.2018.03.001 |
Publisher version: | http://dx.doi.org/10.1016/j.pharmthera.2018.03.001 |
Language: | English |
Additional information: | This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions. |
Keywords: | Alzheimer's disease, beta-Amyloid, Degu, Neurodegeneration, Neuroinflammation, Octodon degus, MILD COGNITIVE IMPAIRMENT, CENTRAL-NERVOUS-SYSTEM, DUAL-PHASING RODENT, NATURAL MODEL, MELATONIN SYNTHESIS, DIURNAL RODENT, RISK-FACTORS, MEMANTINE, INSULIN, BRAIN |
UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Movement Neurosciences |
URI: | https://discovery.ucl.ac.uk/id/eprint/10124345 |
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