Translating the MAM Model of Psychosis to Humans
Identifieur interne : 000B03 ( Main/Exploration ); précédent : 000B02; suivant : 000B04Translating the MAM Model of Psychosis to Humans
Auteurs : Gemma Modinos [Royaume-Uni] ; Paul Allen [Royaume-Uni] ; Anthony A. Grace [États-Unis] ; Philip Mcguire [Royaume-Uni]Source :
- Trends in neurosciences [ 0166-2236 ] ; 2014.
Descripteurs français
- KwdFr :
- MESH :
- anatomopathologie : Encéphale, Troubles psychotiques.
- physiopathologie : Encéphale, Troubles psychotiques.
- Acétate de méthyl-ONN-azoxy-méthyle, Animaux, Humains, Modèles animaux de maladie humaine.
English descriptors
- KwdEn :
- MESH :
- chemical : Methylazoxymethanol Acetate.
- pathology : Brain, Psychotic Disorders.
- physiopathology : Brain, Psychotic Disorders.
- Animals, Disease Models, Animal, Humans.
Abstract
Elevated dopamine function and alterations in the medial temporal lobe structure and function (MTL) are two of the most robust findings in schizophrenia, but how interactions between these abnormalities underlie the onset of psychosis is unclear. Although several preclinical models of psychosis have been proposed, the methylazoxymethanol acetate (MAM) rodent model provides a mechanistic account linking these two clinical observations. The model proposes that psychosis develops as a result of a perturbation of MTL function, leading to elevated striatal dopamine dysfunction. We review a number of recent neuroimaging studies that examine components of the putative model in people with an ultra high risk (UHR) of psychosis. Whilst data from these studies are broadly consistent with the MAM model, that the potential for comparing various kinds of neurobiological data across animal and human studies imposes some limitations on what can be inferred from these data. Going forward, longitudinal studies are needed to explicitly test the model’s predictions in UHR populations.
Url:
DOI: 10.1016/j.tins.2014.12.005
PubMed: 25554679
PubMed Central: 4455929
Affiliations:
- Royaume-Uni, États-Unis
- Angleterre, Grand Londres, Pennsylvanie
- Londres, Pittsburgh
- Université de Pittsburgh
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Le document en format XML
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Although several preclinical models of psychosis have been proposed, the methylazoxymethanol acetate (MAM) rodent model provides a mechanistic account linking these two clinical observations. The model proposes that psychosis develops as a result of a perturbation of MTL function, leading to elevated striatal dopamine dysfunction. We review a number of recent neuroimaging studies that examine components of the putative model in people with an ultra high risk (UHR) of psychosis. Whilst data from these studies are broadly consistent with the MAM model, that the potential for comparing various kinds of neurobiological data across animal and human studies imposes some limitations on what can be inferred from these data. Going forward, longitudinal studies are needed to explicitly test the model’s predictions in UHR populations.</p></div></front></TEI><affiliations><list><country><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Grand Londres</li><li>Pennsylvanie</li></region><settlement><li>Londres</li><li>Pittsburgh</li></settlement><orgName><li>Université de Pittsburgh</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Modinos, Gemma" sort="Modinos, Gemma" uniqKey="Modinos G" first="Gemma" last="Modinos">Gemma Modinos</name></region><name sortKey="Allen, Paul" sort="Allen, Paul" uniqKey="Allen P" first="Paul" last="Allen">Paul Allen</name><name sortKey="Mcguire, Philip" sort="Mcguire, Philip" uniqKey="Mcguire P" first="Philip" last="Mcguire">Philip Mcguire</name></country><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Grace, Anthony A" sort="Grace, Anthony A" uniqKey="Grace A" first="Anthony A." last="Grace">Anthony A. 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