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OBJECTIVE:To investigate the relation between head trauma and incidence of dementia in a prospective population-based study. BACKGROUND:Whether head trauma increases the risk of dementia and AD remains controversial. It has been suggested that the risk might be particularly increased for carriers of the APOE-epsilon4 allele. METHODS:The study population included 6645 participants of the prospective population-based Rotterdam Study, aged 55 years or older, who were free of dementia at baseline. Head trauma with loss of consciousness was measured at baseline by a self-report to a physician and detailed the number of head traumas, time since head trauma, and duration of loss of consciousness. The cohort was followed for incident dementia that was diagnosed according to international criteria. Logistic regression was used to calculate the risk of dementia after adjusting for age, gender, and education. RESULTS:No increased risk of dementia or AD was found for persons with a history of head trauma with loss of consciousness (relative risk [RR] for dementia = 1.0, 95% CI, 0.5-2.0; RR for AD = 0.8, 95% CI, 0.4-1.9). Multiple head traumas, time since head trauma, and duration of unconsciousness did not significantly influence the risk of dementia. In addition, the APOE-epsilon4 allele did not modify the relationship. CONCLUSIONS:This study suggests that mild head trauma is not a major risk factor for dementia or AD in the elderly. In addition, this study does not concur with previous cross-sectional studies suggesting an interaction with the APOE genotype.

Original publication

DOI

10.1212/wnl.53.9.1959

Type

Journal article

Journal

Neurology

Publication Date

12/1999

Volume

53

Pages

1959 - 1962

Addresses

Department of Epidemiology and Biostatistics, Erasmus University Medical School, Rotterdam, The Netherlands.

Keywords

Humans, Brain Injury, Chronic, Alzheimer Disease, Apolipoproteins E, Risk, Cohort Studies, Prospective Studies, Genotype, Aged, Aged, 80 and over, Urban Population, Netherlands, Female, Male, Apolipoprotein E4