Translating the MAM model of psychosis to humans

Gemma Modinos1, Paul Allen1, Anthony A Grace2

  • 1Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Trends in Neurosciences
|January 3, 2015
PubMed

Insights

Schizophrenia research suggests medial temporal lobe (MTL) changes and dopamine dysfunction may interact to cause psychosis. Human studies in individuals at ultra-high risk (UHR) show findings consistent with the methylazoxymethanol acetate (MAM) model.

Area of Science:

  • Neuroscience
  • Psychiatry
  • Neuroimaging

Background:

  • Schizophrenia is characterized by elevated dopamine function and medial temporal lobe (MTL) structural/functional alterations.
  • The interplay between these abnormalities in psychosis onset remains poorly understood.
  • The methylazoxymethanol acetate (MAM) rodent model links MTL dysfunction to striatal dopamine abnormalities.

Purpose of the Study:

  • To review neuroimaging studies investigating components of the MAM model in humans.
  • To examine human data from individuals at ultra-high risk (UHR) for psychosis.
  • To assess the consistency of human findings with the MAM rodent model.

Main Methods:

  • Review of recent neuroimaging studies.
  • Focus on human participants with ultra-high risk (UHR) for psychosis.
  • Comparison of human neuroimaging data with predictions from the MAM model.

Main Results:

  • Neuroimaging findings in UHR individuals are broadly consistent with the MAM model's proposed mechanisms.
  • Evidence supports a link between MTL alterations and dopamine system dysfunction in psychosis development.
  • Specific components of the MAM model are supported by human data.

Conclusions:

  • Human neuroimaging data align with the MAM model's hypothesis regarding psychosis development.
  • The MAM model provides a useful framework for understanding schizophrenia pathophysiology.
  • Further research is needed to refine cross-species comparisons and fully validate the model in humans.

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