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4 allele
From the Departments of Psychology (J.P., L.N.), Radiation Sciences–Radiation Physics (A.L.), and Clinical Sciences and Psychiatry (R.A.), Umeå University, Sweden; Department of Psychology (J.P.), University of Michigan, Ann Arbor; MR Research Center (J.L., M.I.), Karolinska Hospital, Stockholm, Sweden; Department of Molecular Genetics VIB8 (M.C., C.V.B.), University of Antwerp, Belgium; and Department of Psychology (L.-G.N.), Stockholm University, Sweden.
Address correspondence and reprint requests to Dr. Persson, Department of Psychology, Umeå University, S-901 87 Umeå, Sweden; e-mail: perssonj{at}umich.edu
Background: Previous research has shown that polymorphisms of apolipoprotein E (APOE) represent genetic risk factors for dementia and for cognitive impairment in the elderly. The neural mechanisms by which these genetic variations influence behavioral performance or clinical severity are not well understood.
Methods: The authors used diffusion tensor imaging to investigate ultrastructural properties in brain white matter to detect pathologic processes that modify tissue integrity. Sixty participants were included in the study of which 30 were homozygous for the APOE 
3 allele, 10 were homozygous for the APOE 4 allele, and 20 had the APOE 34 allele combination. All individuals were non-demented, and the groups were matched on demographic variables and cognitive performance.
Results: The results showed a decline in fractional anisotropy, a marker for white matter integrity, in the posterior corpus callosum of 4 carriers compared to non-carriers. Additional sites of altered white matter integrity included the medial temporal lobe.
Conclusions: Although the mechanism underlying vulnerability of white matter tracts in APOE 4 carriers is still unknown, these findings suggest that increased genetic risk for developing Alzheimer disease is associated with changes in microscopic white matter integrity well before the onset of dementia.
Disclosure: The authors report no conflicts of interest.
Received May 10, 2005. Accepted in final form December 19, 2005.
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