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Striatal dopamine synthesis capacity in twins discordant for schizophrenia

  • P. Shotbolt (a1), P. R. Stokes (a1), S. F. Owens (a2), T. Toulopoulou (a2), M. M. Picchioni (a2) (a3), S. K. Bose (a1), R. M. Murray (a2) and O. D. Howes (a1) (a2)...
Abstract
Background

Elevated striatal dopamine synthesis capacity is thought to be fundamental to the pathophysiology of schizophrenia and has also been reported in people at risk of psychosis. It is therefore unclear if striatal hyperdopaminergia is a vulnerability marker for schizophrenia, or a state feature related to the psychosis itself. Relatives of patients with schizophrenia are themselves at increased risk of developing the condition. In this study we examined striatal dopamine synthesis capacity in both members of twin pairs discordant for schizophrenia.

Method

In vivo striatal dopamine synthesis capacity was examined using fluorine-18-l-dihydroxyphenylalanine (18F-DOPA) positron emission tomography (PET) scans in seven twin pairs discordant for schizophrenia and in a control sample of 10 healthy control twin pairs.

Results

Striatal 18F-DOPA uptake was not elevated in the unaffected co-twins of patients with schizophrenia (p=0.65) or indeed in the twins with schizophrenia (p=0.89) compared to the control group. Levels of psychotic symptoms were low in the patients with schizophrenia who were in general stable [mean (s.d.) Positive and Negative Syndrome Scale (PANSS) total=56.8 (25.5)] whereas the unaffected co-twins were largely asymptomatic.

Conclusions

Striatal dopamine synthesis capacity is not elevated in symptom-free individuals at genetic risk of schizophrenia, or in well-treated stable patients with chronic schizophrenia. These findings suggest that striatal hyperdopaminergia is not a vulnerability marker for schizophrenia.

Copyright
Corresponding author
*Address for correspondence: Dr P. Shotbolt, Clinical Imaging Centre, Imperial College London, Du Cane Road, London W12 0NN, UK. (Email: p.shotbolt@imperial.ac.uk)
Linked references
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This list contains references from the content that can be linked to their source. For a full set of references and notes please see the PDF or HTML where available.

A Dagher , R Gunn , G Lockwood , VJ Cunningham , PM Grasby , DJ Brooks (1998). Measuring neurotransmitter release with PET: methodological issues. In Quantitative Functional Brain Imaging with Positron Emission Tomography(ed. R. Carson , M. Daube-Witherspoon and P. Herscovitch ), pp. 449454. Academic Press: San Diego.

WR Martin , MR Palmer , CS Patlak , DB Calne (1989). Nigrostriatal function in humans studied with positron emission tomography. Annals of Neurology 26, 535542.

D Mamo , S Kapur , CM Shammi , G Papatheodorou , S Mann , F Therrien , G Remington (2004). A PET study of dopamine D2 and serotonin 5-HT2 receptor occupancy in patients with schizophrenia treated with therapeutic doses of ziprasidone. American Journal of Psychiatry 161, 818825.

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Psychological Medicine
  • ISSN: 0033-2917
  • EISSN: 1469-8978
  • URL: /core/journals/psychological-medicine
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