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From the Alzheimers Disease Research Center (Drs. Johnson, Morris, Galvin) and Departments of Neurology (Drs. Johnson, Morris, Galvin), Pathology and Immunology (Dr. Morris), and Anatomy and Neurobiology (Dr. Galvin), Washington University School of Medicine, St. Louis, MO.
Address correspondence and reprint requests to Dr. James E. Galvin, Alzheimer Disease Research Center, Washington University School of Medicine, 4488 Forest Park, Suite 130, St. Louis, MO 63108; e-mail: galvinj{at}neuro.wustl.edu
Objective: To investigate the cognitive decline in dementia with Lewy bodies (DLBs) and characterize the contribution of Lewy bodies (LBs) to cognitive impairment in the presence of concurrent Alzheimer disease (AD).
Methods: Cognitive deficits and rates of progression attributable to DLB and AD neuropathology were investigated in three groups of participants from the longitudinal cohort of the Alzheimer Disease Research Center at Washington University with autopsy-confirmed diagnoses of pure DLB (n = 9), mixed DLB/AD (n = 57), and pure AD (n = 66). Factor analysis was used to recover latent constructs in a comprehensive psychometric test battery, analysis of variance was used to test group differences on the observed dimensions, and random effects models were used to test longitudinal rates of cognitive decline.
Results: Patients with AD pathology performed worse on the verbal memory dimension. Patients with LB pathology performed worse on the visuospatial dimension. Combined pathology affected visuospatial performance but not verbal memory. The rate of cognitive decline in the DLB, DLB/AD combined, and the pure AD groups was equivalent.
Conclusions: The comorbid presence of DLB and AD alters the cognitive presentation of visuospatial deficits in dementia but does not alter dementia progression. Both visuospatial and verbal abilities declined at similar rates across the three patient groups. DLB diagnosis may be improved, particularly when there is comorbid AD, by using domain-specific testing.
Supported by grants from the National Institute on Aging (AG20764 [J.E.G.], AG03991 [J.C.M.], and AG05681 [J.C.M.]) and the American Federation for Aging Research [JEG]. Dr. Galvin is a recipient of the Paul Beeson Physician Faculty Scholar Award in Aging Research. This project was also supported by generous gifts from the Alan A. and Edith L. Wolff Charitable Trust and the Blue Gator Foundation to the ADRC and Dr. Galvin.
Disclosure: The authors report no conflicts of interest.
Received February 12, 2005. Accepted in final form July 8, 2005.
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