Background: Lewy bodies (LB) are a frequent coexisting pathology in symptomatic Alzheimer disease (AD). The influence of LB pathology on the clinical phenotype of AD has been investigated but with inconsistent results. The purpose of this project was to determine whether the presence of LB pathology is associated with the clinical phenotypes before death among longitudinally assessed participants found to have AD at autopsy. Methods: A total of 531 participants who met neuropathologic criteria for intermediate or high "likelihood" of AD according to the National Institute on Aging-Ronald Reagan Institute guidelines were enrolled in the National Alzheimer's Coordinating Center (NACC) database. All participants had a clinical assessment within two years of death. We examined demographic features such as age at onset, age at death, gender, education, disease duration, APOE epsilon4 status, plaques (diffuse and neuritic) frequency and tangles stage. We also obtained the Clinical Dementia Rating-Sum of Boxes (CDR-SB), Unified Parkinson's Disease Rating Scale motor score (mUPDRS) and Neuropsychiatric Inventory Questionnaire (NPI-Q). Chi-square and t-tests were used for unadjusted analyses and general linear models were used for adjusted analyses. Results: Age at onset and age at death were lower among AD participants with concomitant LBs than those without LB pathology. Men more often had LB pathology. Participants with LBs more often had at least one APOE epsilon4 allele. After adjustment for age, gender, education, neuritic and diffuse plaque frequency, and tangle stage, scores on the NPI-Q and the mUPDRS were more impaired for participants who had comorbid LB pathology. After additional adjustment of APOE epsilon4 status, only the mUPDRS showed significantly higher scores among persons who had both AD and LB pathology compared to the group that had AD without LBs. Conclusions: Participants with both AD and LB pathology have a clinical phenotype which may be distinguished from AD alone. The identification of comorbidity in the absence of reliable biomarkers of alpha-synuclein pathology may eventually help in the selection of patients for specific drug therapy.
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