Dementia, quantitative neuroimaging, and apolipoprotein E genotype

Citation
Ed. Bigler et al., Dementia, quantitative neuroimaging, and apolipoprotein E genotype, AM J NEUROR, 21(10), 2000, pp. 1857-1867
Citations number
95
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging","Neurosciences & Behavoir
Journal title
AMERICAN JOURNAL OF NEURORADIOLOGY
ISSN journal
01956108 → ACNP
Volume
21
Issue
10
Year of publication
2000
Pages
1857 - 1867
Database
ISI
SICI code
0195-6108(200011/12)21:10<1857:DQNAAE>2.0.ZU;2-5
Abstract
BACKGROUND AND PURPOSE: Quantitative MR imaging differences in an elderly p opulation of subjects with various clinical disorders (including dementia, particularly Alzheimer's disease and vascular dementia) and disorders of mi ld cognitive impairment were examined. Potential quantitative MR difference s were assessed by presence or absence of the apolipoprotein E (APOE) epsil on4 allele and by level of cognitive deficit. METHODS: One hundred eighty subjects with a diagnosis of dementia or other clinical disorders were identified from an eligible population of 5677 elde rly individuals. Age, duration of disease, and head size (where appropriate ) were considered as covariates. APOE genotype was determined by polymerase chain reaction using buccal material. Axial and coronal intermediate- and T2-weighted MR images were quantified using a multispectral segmentation al gorithm. Cognitive status was assessed by means of a modified Mini-Mental S tatus Examination. RESULTS: All types of dementing illness showed significant volume reduction s in the majority of structures examined, particularly in the total brain, hippocampus, and white and gray matter, and increased CSF and ventricular v olumes. Subjects with mild cognitive impairment showed fewer atrophic chang es but were still distinguishable from the 24 control subjects. Presence of an epsilon4 allele was associated with smaller hippocampal volume in subje cts with Alzheimer's disease and vascular dementia within just 1 year of di sease onset. For other analyses, atrophy related to the presence of the eps ilon4 allele disappeared after controlling for age and length of disease. CONCLUSION: The effects of the epsilon4 allele on brain morphology may be s ubtly expressed early in the development of dementia, but do not specifical ly affect cerebral atrophy thereafter. Cognitive impairment is associated w ith atrophy irrespective of diagnosis and presence of epsilon4.