American Journal of Neuroradiology 21:1857-1868 (11 2000)
© 2000 American Society of Neuroradiology
ARTICLE
Dementia, Quantitative Neuroimaging, and Apolipoprotein E Genotype
a From the Department of Psychology and Neuroscience, 1001 SWKT, Brigham Young University, Provo, UT 84602. Address reprint requests to Erin D. Bigler, PhD.
BACKGROUND AND PURPOSE: Quantitative MR imaging differences in an elderly population of subjects with various clinical disorders (including dementia, particularly Alzheimer's disease and vascular dementia) and disorders of mild cognitive impairment were examined. Potential quantitative MR differences were assessed by presence or absence of the apolipoprotein E (APOE) 
4 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 elderly 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 algorithm. Cognitive status was assessed by means of a modified Mini-Mental Status Examination.
RESULTS: All types of dementing illness showed significant volume reductions in the majority of structures examined, particularly in the total brain, hippocampus, and white and gray matter, and increased CSF and ventricular volumes. Subjects with mild cognitive impairment showed fewer atrophic changes but were still distinguishable from the 24 control subjects. Presence of an 4 allele was associated with smaller hippocampal volume in subjects with Alzheimer's disease and vascular dementia within just 1 year of disease onset. For other analyses, atrophy related to the presence of the 4 allele disappeared after controlling for age and length of disease.
CONCLUSION: The effects of the 4 allele on brain morphology may be subtly expressed early in the development of dementia, but do not specifically affect cerebral atrophy thereafter. Cognitive impairment is associated with atrophy irrespective of diagnosis and presence of 4.
This article has been cited by other articles:
 |
|
 |
|
  S. M. Nestor, R. Rupsingh, M. Borrie, M. Smith, V. Accomazzi, J. L. Wells, J. Fogarty, R. Bartha, and the Alzheimer's Disease Neuroimaging Initiative Ventricular enlargement as a possible measure of Alzheimer's disease progression validated using the Alzheimer's disease neuroimaging initiative database Brain, September 1, 2008; 131(9): 2443 - 2454. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. Zhong, M. Ewers, S. Teipel, K. Burger, A. Wallin, K. Blennow, P. He, C. McAllister, H. Hampel, and Y. Shen Levels of beta-Secretase (BACE1) in Cerebrospinal Fluid as a Predictor of Risk in Mild Cognitive Impairment Arch Gen Psychiatry, June 1, 2007; 64(6): 718 - 726. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. Lane and M. R. Farlow Lipid homeostasis and apolipoprotein E in the development and progression of Alzheimer's disease J. Lipid Res., May 1, 2005; 46(5): 949 - 968. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. R. Farlow, Y. He, S. Tekin, J. Xu, R. Lane, and H. C. Charles Impact of APOE in mild cognitive impairment Neurology, November 23, 2004; 63(10): 1898 - 1901. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. S.C. Korf, L. R. White, P. Scheltens, and L. J. Launer Midlife Blood Pressure and the Risk of Hippocampal Atrophy: The Honolulu Asia Aging Study Hypertension, July 1, 2004; 44(1): 29 - 34. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. De Stefano, M. L. Bartolozzi, B. Nacmias, V. Zipoli, M. Mortilla, L. Guidi, G. Siracusa, S. Sorbi, A. Federico, and M. P. Amato Influence of Apolipoprotein E {epsilon}4 Genotype on Brain Tissue Integrity in Relapsing-Remitting Multiple Sclerosis Arch Neurol, April 1, 2004; 61(4): 536 - 540. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Hirono, M. Hashimoto, M. Yasuda, H. Kazui, and E. Mori Accelerated Memory Decline in Alzheimer's Disease With Apolipoprotein {epsilon}4 Allele J Neuropsychiatry Clin Neurosci, August 1, 2003; 15(3): 354 - 358. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R J L Walters, N C Fox, J M Schott, W R Crum, J M Stevens, M N Rossor, and D J Thomas Transient ischaemic attacks are associated with increased rates of global cerebral atrophy J. Neurol. Neurosurg. Psychiatry, February 1, 2003; 74(2): 213 - 216. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Yount, K. A. Raschke, M. Biru, D. F. Tate, M. J. Miller, T. Abildskov, P. Gandhi, D. Ryser, R. O. Hopkins, and E. D. Bigler Traumatic Brain Injury and Atrophy of the Cingulate Gyrus J Neuropsychiatry Clin Neurosci, November 1, 2002; 14(4): 416 - 423. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Hirono, M. Hashimoto, M. Yasuda, K. Ishii, S. Sakamoto, H. Kazui, and E. Mori The effect of APOE {epsilon}4 allele on cerebral glucose metabolism in AD is a function of age at onset Neurology, March 12, 2002; 58(5): 743 - 750. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. D. Bigler, C. V. Andersob, and D. D. Blatter Temporal Lobe Morphology in Normal Aging and Traumatic Brain Injury AJNR Am. J. Neuroradiol., February 1, 2002; 23(2): 255 - 266. [Abstract] [Full Text] [PDF]
|
|