| 1. |
- Lind, J., et al.
(författare)
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Parietal cortex activation predicts longitudinal memory decline in APOE ε4 carriers.
- 2006
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Ingår i: NeuroReport. ; :17, s. 1683-1686
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Tidskriftsartikel (populärvet., debatt m.m.)abstract
- Apolipoprotein E-epsilon 4 is the main known genetic risk factor for Alzheimer’s disease. Functional abnormalities in the parietal cortex have been reported for Alzheimer’s disease patients and also for those at risk. Hence, a critical question is whether measurements of parietal cortex integrity may predict negative outcome among at- risk persons. We studied nondemented apolipo-protein E-epsilon 4 carriers and found a significant relationship between parietal blood-oxygen-level-dependent functional magnetic resonance imaging response during a word categorization task and subsequent episodic memory performance. Thus, the results show that parietal cortex alterations predict memory decline in nondemented apolipoprotein E-epsilon 4 carriers, and hence likely progression to Alzheimer’s disease.
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| 2. |
- Persson, J, et al.
(författare)
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Altered brain white-matter integrity in non-demented carriers of the APOE ε4 allele: A risk for Alzheimer’s disease.
- 2006
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Ingår i: Neurology. - : Ovid Technologies (Wolters Kluwer Health). - 0028-3878 .- 1526-632X. ; 66:7, s. 1029-1033
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Tidskriftsartikel (refereegranskat)abstract
- Previous research has shown that polymorphisms of the 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. We used diffusion tensor imaging to investigate ultrastructural properties in brain white-matter to detect pathological processes that modify tissue integrity. Sixty participants were included in the study of which 30 were homozygous for the APOE ε3 allele, 10 were homozygous for the APOE ε4 allele, and 20 had the APOE ε34 allele combination. All individuals were non-demented, and the groups were matched on demographic variables and cognitive performance. The results showed a decline in fractional anisotropy, a marker for white-matter integrity, in the posterior corpus callosum of ε4 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 ε4 carriers is still unknown, our findings suggest that increased genetic risk for developing AD is associated with changes in microscopic white-matter integrity well before the onset of dementia.
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