<i>Octodon degus</i>: A Model for the Cognitive Impairment Associated with <scp>A</scp>lzheimer's Disease

Tarragon, Ernesto; López, Dolores; Estrada, Cristina; Ana, Gonzalez-Cuello; Schenker, Esther; Pifferi, Fabien; Bordet, Régis; Richardson, Jill C.; Herrero, M.T.

doi:10.1111/cns.12125

Cited by 41 publications

(40 citation statements)

References 74 publications

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“…These studies highlight the therapeutic potential of the induction of TMS in O. degus. Taking into consideration that this rodent constitutes a "spontaneous" model of neurological disorders such as Alzheimer´s disease (Tarragon et al, 2013), it holds a significant promise to progress in the comprehension of brain mechanisms and to originate novel …”

Section: Discussionmentioning

confidence: 99%

“…Analyzing memory impairment caused by this challenge in the O. degus is particularly important and considerable, since this social rodent has become an increasingly familiar and accepted experimental animal in the latest years. Furthermore, many therapeutic and medical disciplines, particularly those referred to brain functions, has characterized as an important animal model for research (Tarragon et al, 2013). We used SD as a condition which alters the formation and expression of memories and originates a failure in both procedural and declarative memories (Walker and Stickgold, 2004) (Jugovac and Cavallero, 2012) (Huber et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Cognitive Impairment After Sleep Deprivation Rescued by Transcranial Magnetic Stimulation Application in Octodon degus

et al. 2015

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Sleep is indispensable for maintaining regular daily life activities and a fundamental physiological purpose in cognitive performance. Sleep deprivation (SD) may affect subsequent learning capacity and ability to constitute new memories, particularly in the situation of hippocampusdependent tasks. Transcranial magnetic stimulation (TMS) is a non-invasive procedure of electromagnetic induction that generates electric currents activating nearby nerve cells in the stimulated cortical area. Several studies have begun to therapeutically use TMS. The present study was designed to evaluate how TMS could improve learning and memory functions after SD in O. degus. Thirty juvenile (aged eighteen months old) females were divided in three groups (control, acute and chronic TMS treatment -with and without SD). To immobilize TMS-treated groups, they were disposed in plastic cylindrical while the O. degus were receiving head magnetic stimulation. SD was achieved by gently handling the animals to keep them awake during the night. Behavioral tests include Radial Arm Maze (RAM), Barnes Maze (BM) and Novel Object Recognition (NOR). When TMS treatment was applied during several days, there was significant improvement of cognitive performance after SD. Noteworthy, only one session of TMS is able to improve some parameters related with spatial memory. No side effects were observed. After SD, chronic TMS treatment provokes significant amelioration in learning and in both spatial and working memory. Nonetheless, an acute treatment of TMS is already sufficient to improve spatial memory. To our knowledge, in this manuscript we confirm that sleep deprivation (SD) results in cognitive impairment measured with 3 different psychological tests, and we provide the evidence that transcranial magnetic stimulation (TMS) treatment significantly improve cognitive performance in sleep-deprived animals. Then, after SD, TMS can improve learning, spatial memory and working memory functions.We feel that these exciting results are novel and important, and can be of interest for scientists, neurologists and physicians working on sleep pathologies.The experimental work was done in compliance with the National Research Council's Guide for the care and use of laboratory animals, and the Guidelines promulgated by the European Communities Council Directive 2010/63/ECC.The data presented in the manuscript are original and the manuscript is not under consideration elsewhere. None of the manuscript contents has been previously published. In the present work we do not have any conflict of financial interest.All authors have seen and approved the manuscript.Trusting you will consider our manuscript worthy of review by your Journal, Yours truly, there was significant improvement of cognitive performance after SD. María-Trinidad HerreroNoteworthy, only one session of TMS is able to improve some parameters related with spatial memory. No side effects were observed. After SD, chronic TMS treatment provokes significant amelioration in learning and in both spat...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cognitive Impairment After Sleep Deprivation Rescued by Transcranial Magnetic Stimulation Application in Octodon degus

et al. 2015

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“…Recently, it has been revealed that NFT composed of hyperphosphorylated tau form in the brains of domestic cats, Tsushima leopard cats, and degus, 24,28,187 which cannot be explained by the brain aging speed hypothesis. Table 2 summaries the Ab amino acid sequences of various animals.…”

Section: Alzheimer's Diseasementioning

confidence: 99%

Pathology of the Aging Brain in Domestic and Laboratory Animals, and Animal Models of Human Neurodegenerative Diseases

et al. 2016

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According to the WHO, the proportion of people over 60 years is increasing and expected to reach 22% of total world's population in 2050. In parallel, recent animal demographic studies have shown that the life expectancy of pet dogs and cats is increasing. Brain aging is associated not only with molecular and morphological changes but also leads to different degrees of behavioral and cognitive dysfunction. Common age-related brain lesions in humans include brain atrophy, neuronal loss, amyloid plaques, cerebrovascular amyloid angiopathy, vascular mineralization, neurofibrillary tangles, meningeal osseous metaplasia, and accumulation of lipofuscin. In aging humans, the most common neurodegenerative disorder is Alzheimer's disease (AD), which progressively impairs cognition, behavior, and quality of life. Pathologic changes comparable to the lesions of AD are described in several other animal species, although their clinical significance and effect on cognitive function are poorly documented. This review describes the commonly reported age-associated neurologic lesions in domestic and laboratory animals and the relationship of these lesions to cognitive dysfunction. Also described are the comparative interspecies similarities and differences to AD and other human neurodegenerative diseases including Parkinson's disease and progressive supranuclear palsy, and the spontaneous and transgenic animal models of these diseases.

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“…AD, a neurodegenerative disease, is one of the most common and multifactorial forms of dementia characterized by multiple cognitive impairments, personality changes, and abnormal behavior 2 . The key pathological emblems observed in AD brain tissues are amyloid beta (Aβ ) peptide and hyperphosphorylated tau (p-tau) protein, although the exact mechanisms which cause these alterations are yet to be uncovered 3 . The formation of Aβ is due to the aggregation of extracellular senile plaques (SP), while neurofibrillary tangles (NFTs) are caused by abnormal deposits of p-tau proteins 3 .…”

Section: Introductionmentioning

confidence: 99%

Chemicals used for the induction of Alzheimer’s disease-like cognitive dysfunctions in rodents

et al. 2019

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Alzheimer's disease (AD) is the most frequent and multifactorial form of dementia, characterised by multiple cognitive impairments and personality changes. Different methods including chemicals have been used to induce AD-like symptoms in rodent in order to screen many therapeutic drugs for a variety of cognitive dysfunctions. Articles from reliable databases such as Google Scholar, Science Direct, PubMed, Scopus, and Ovid were searched and retrieved with the following descriptors: 'Alzheimer's Disease' , Cognitive impairments' , Neurotoxins that induce AD' , Alzheimerogenic chemicals' , excitotoxins' , Amyloid beta' , neurofibrillary tangles. A number of chemicals have been studied to develop an animal model of AD on the basis of their mechanism of action for cognitive dysfunctions. Some of such chemicals are Heavy metals, Scopolamine, Ethanol, Colchicine, Streptozotocin, Lipopolysaccharide, and Okadaic acid among others, with a view to understanding the pathogenesis of this devastating disease. The purpose of this review is to put forward some AD pathophysiology including AD causative theories and also highlight some Alzheimerogenic chemicals for the purpose of enriching our existing knowledge. It is worth mentioning that not all the biochemical, histopathological, cognitive and behavioural abnormalities can be recapitulated. Nonetheless, experimental models of AD produced by chemicals offer insights to unravelling the pathogenesis of the disease.

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Octodon degus: A Model for the Cognitive Impairment Associated with Alzheimer's Disease

Cited by 41 publications

References 74 publications

Cognitive Impairment After Sleep Deprivation Rescued by Transcranial Magnetic Stimulation Application in Octodon degus

Cognitive Impairment After Sleep Deprivation Rescued by Transcranial Magnetic Stimulation Application in Octodon degus

Pathology of the Aging Brain in Domestic and Laboratory Animals, and Animal Models of Human Neurodegenerative Diseases

Chemicals used for the induction of Alzheimer’s disease-like cognitive dysfunctions in rodents

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