Voxel-based analysis of cerebral glucose metabolism in mono- and dizygotic twins discordant for Alzheimer disease
- J J Virta1,
- S Aalto1,2,
- T Järvenpää1,
- M Karrasch2,
- J Kaprio3,4,
- M Koskenvuo3,
- I Räihä5,6,
- T Viljanen1,
- J O Rinne1
- 1Turku PET Centre, University of Turku, Turku, Finland
- 2Department of Psychology, Åbo Akademi University, Turku, Finland
- 3Department of Public Health, University of Helsinki, Finland
- 4Department of Mental Health and Alcohol Research National Public Health Institute, Helsinki, Finland
- 5Department of Geriatrics, University of Turku, Finland
- 6Department of Geriatrics, Turku City Hospital, Finland
- Mr J J Virta, Turku PET Centre, University of Turku, PO Box 52, FIN-20521 Turku, Finland; jyri.virta{at}utu.fi
- Received 24 January 2008
- Revised 31 August 2008
- Accepted 16 September 2008
- Published Online First 31 October 2008
Abstract
Background: Sporadic Alzheimer disease (AD) is a multifactorial disease to which both genetic and environmental factors contribute. Therefore, twin pairs are useful in studying its pathogenesis and aetiology. Cerebral glucose metabolism has been found to be reduced in AD patients.
Methods: Cerebral glucose metabolism was studied in seven monozygotic (MZ) and nine same-sexed dizygotic (DZ) twin pairs discordant for AD using positron emission tomography. To obtain objective and explorative results concerning differences in glucose metabolism, the analysis was performed utilising modern voxel-based analysis methodology statistical parametric mapping and automated region-of-interest analysis.
Results: In the demented MZ and DZ co-twins, cerebral glucose metabolism was extensively reduced compared with controls. The non-demented MZ co-twins showed reduced metabolism in inferior frontal, lateral temporal, parietal and medial temporal cortices as well as in the thalamus, putamen and right amygdala. In contrast, no reductions were found in the non-demented DZ co-twins. The reduction found in the non-demented MZ co-twins may be an indicator of genetic susceptibility to AD.
Footnotes
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Competing interests: None.
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Ethics approval: Ethics approval was provided by the Joint Ethical Committee of the University of Turku and the Turku University City Hospital.
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Patient consent: Obtained.








