 |
 |

White Matter Lesions Are Prevalent but Differentially Related With Cognition in Aging and Early Alzheimer Disease
Jeffrey M. Burns, MD;
Jessica A. Church, BS;
David K. Johnson, PhD;
Chengjie Xiong, PhD;
Daniel Marcus, PhD;
Anthony F. Fotenos, BS;
Abraham Z. Snyder, MD;
John C. Morris, MD;
Randy L. Buckner, PhD
Arch Neurol. 2005;62:1870-1876.
Background White matter lesions (WMLs) are prevalent in nondemented aging and in Alzheimer disease (AD). Their relationship with cognition in the earliest stages of AD is unknown.
Objective To assess the relationship between WMLs and cognition in nondemented aging and in early-stage AD.
Design Cross-sectional study.
Setting Alzheimer Disease Research Center, St Louis, Mo.
Participants Participants were nondemented (n = 88) or had very mild (n = 48) or mild (n = 20) AD.
Main Outcome Measures Regression coefficients for deep WMLs and periventricular WMLs (PVWMLs) as predictors of cognition, after controlling for age, educational achievement, brain atrophy, and infarctlike lesions.
Results White matter lesions were present in nondemented aging and in early-stage AD, with no group differences in deep WML burden and a modest PVWML burden increase in the AD group. The prevalence of infarctlike lesions was equivalent between groups. Age and hypertension were related to deep WML burden and PVWML burden. Deep WML burden and PVWML burden were associated with reduced global cognition in AD but not in nondemented aging. A PVWML x AD status interaction for global cognition suggests that the relationship between PVWMLs and cognition is modified by AD. In AD, global cognitive reductions were related to impairments in visual memory, processing speed, and executive function.
Conclusions White matter lesions are prevalent in nondemented aging and in early-stage AD, and their presence influences cognitive impairment in the earliest stages of AD. Individuals with early-stage AD may be more vulnerable to the cognitive effect of WMLs than nondemented aging individuals with similar WML burden.
Author Affiliations: Departments of Neurology (Drs Burns, Johnson, Snyder, and Morris and Ms Church), Biostatistics (Drs Xiong and Buckner), Psychology (Dr Marcus and Mr Fotenos), Radiology (Drs Snyder and Buckner), and Pathology and Immunology (Dr Morris), Alzheimer Disease Research Center (Drs Burns, Johnson, Xiong, and Morris), and Howard Hughes Medical Institute (Drs Marcus and Buckner), Washington University, St Louis, Mo. Dr Burns is now with the Department of Neurology, University of Kansas School of Medicine, Kansas City.
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
 |
Peripheral ethanolamine plasmalogen deficiency: a logical causative factor in Alzheimer's disease and dementia
Goodenowe et al.
J. Lipid Res. 2007;48:2485-2498.
ABSTRACT
| FULL TEXT
Open Access Series of Imaging Studies (OASIS): Cross-sectional MRI Data in Young, Middle Aged, Nondemented, and Demented Older Adults.
Marcus et al.
J. Cogn. Neurosci. 2007;19:1498-1507.
ABSTRACT
| FULL TEXT
Magnetic Resonance Imaging Predictors of Cognition in Mild Cognitive Impairment
van de Pol et al.
Arch Neurol 2007;64:1023-1028.
ABSTRACT
| FULL TEXT
Cortical microinfarcts and demyelination affect cognition in cases at high risk for dementia
Kovari et al.
Neurology 2007;68:927-931.
ABSTRACT
| FULL TEXT
Poststroke Memory Function in Nondemented Patients: A Systematic Review on Frequency and Neuroimaging Correlates
Snaphaan and de Leeuw
Stroke 2007;38:198-203.
ABSTRACT
| FULL TEXT
Extent and distribution of white matter hyperintensities in normal aging, MCI, and AD
Yoshita et al.
Neurology 2006;67:2192-2198.
ABSTRACT
| FULL TEXT
|