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Traumatic brain injury as a risk factor for Alzheimer disease. Comparison of two retrospective autopsy cohorts with evaluation of ApoE genotype.
BMC Neurol 2001; 1:3BN

Abstract

BACKGROUND AND PURPOSE

The impact of traumatic brain injury (TBI) on the pathogenesis of Alzheimer disease (AD) is still controversial. The aim of our retrospective autopsy study was to assess the impact of TBE and ApoE allele frequency on the development of AD.

MATERIAL AND METHODS

We examined 1. the incidence of AD pathology (Braak stageing, CERAD, NIA-Reagan Institute criteria) in 58 consecutive patients (mean age +/- SD 77.0 +/- 6.8 years) with residual closed TBI lesions, and 2. the frequency of TBI residuals in 57 age-matched autopsy proven AD cases. In both series, ApoE was evaluated from archival paraffin-embedded brain material.

RESULTS

1. TBE series: 12.1 % showed definite and 10.3% probable AD (mean age 77.6 and 75.2 years), only 2/13 with ApoEepsilon3/4. From 45 (77.6%) non-AD cases (mean age 78.2 years), 3 had ApoEepsilon3/4. The prevalence of 22.4% AD in this small autopsy cohort was significantly higher than 3.3% in a recent large clinical series and 14% in the general population over age 70. 2. In the AD cohort with ApoEepsilon4 allele frequency of 30% similar to other AD series, residuals of closed TBI were seen in 4 brains (7%) (mean age +/- SD 78.2 +/- 6.4), all lacking the ApoEepsilon4 allele. TBI incidence was slightly lower than 8.5% in the clinical MIRAGE study.

CONCLUSIONS

The results of this first retrospective autopsy study of TBI, ApoEepsilon allele frequency, and AD confirm clinical studies suggesting severe TBI to be a risk factor for the development AD higher in subjects lacking ApoEepsilon4 alleles. Further studies in larger autopsy series are needed to elucidate the relationship between TBI, genetic predisposition, and AD.

Authors+Show Affiliations

L Boltzmann Institute of Clinical Neurobiology, Baumgartner Hoehe 1, B-Bldg, A-1140 Vienna, Austria. kurt.jellinger@univie.ac.atNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11504565

Citation

Jellinger, K A., et al. "Traumatic Brain Injury as a Risk Factor for Alzheimer Disease. Comparison of Two Retrospective Autopsy Cohorts With Evaluation of ApoE Genotype." BMC Neurology, vol. 1, 2001, p. 3.
Jellinger KA, Paulus W, Wrocklage C, et al. Traumatic brain injury as a risk factor for Alzheimer disease. Comparison of two retrospective autopsy cohorts with evaluation of ApoE genotype. BMC Neurol. 2001;1:3.
Jellinger, K. A., Paulus, W., Wrocklage, C., & Litvan, I. (2001). Traumatic brain injury as a risk factor for Alzheimer disease. Comparison of two retrospective autopsy cohorts with evaluation of ApoE genotype. BMC Neurology, 1, p. 3.
Jellinger KA, et al. Traumatic Brain Injury as a Risk Factor for Alzheimer Disease. Comparison of Two Retrospective Autopsy Cohorts With Evaluation of ApoE Genotype. BMC Neurol. 2001 Dec 18;1:3. PubMed PMID: 11504565.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Traumatic brain injury as a risk factor for Alzheimer disease. Comparison of two retrospective autopsy cohorts with evaluation of ApoE genotype. AU - Jellinger,K A, AU - Paulus,W, AU - Wrocklage,C, AU - Litvan,I, Y1 - 2001/12/18/ PY - 2001/06/29/received PY - 2001/07/30/accepted PY - 2001/8/16/pubmed PY - 2004/1/7/medline PY - 2001/8/16/entrez SP - 3 EP - 3 JF - BMC neurology JO - BMC Neurol VL - 1 N2 - BACKGROUND AND PURPOSE: The impact of traumatic brain injury (TBI) on the pathogenesis of Alzheimer disease (AD) is still controversial. The aim of our retrospective autopsy study was to assess the impact of TBE and ApoE allele frequency on the development of AD. MATERIAL AND METHODS: We examined 1. the incidence of AD pathology (Braak stageing, CERAD, NIA-Reagan Institute criteria) in 58 consecutive patients (mean age +/- SD 77.0 +/- 6.8 years) with residual closed TBI lesions, and 2. the frequency of TBI residuals in 57 age-matched autopsy proven AD cases. In both series, ApoE was evaluated from archival paraffin-embedded brain material. RESULTS: 1. TBE series: 12.1 % showed definite and 10.3% probable AD (mean age 77.6 and 75.2 years), only 2/13 with ApoEepsilon3/4. From 45 (77.6%) non-AD cases (mean age 78.2 years), 3 had ApoEepsilon3/4. The prevalence of 22.4% AD in this small autopsy cohort was significantly higher than 3.3% in a recent large clinical series and 14% in the general population over age 70. 2. In the AD cohort with ApoEepsilon4 allele frequency of 30% similar to other AD series, residuals of closed TBI were seen in 4 brains (7%) (mean age +/- SD 78.2 +/- 6.4), all lacking the ApoEepsilon4 allele. TBI incidence was slightly lower than 8.5% in the clinical MIRAGE study. CONCLUSIONS: The results of this first retrospective autopsy study of TBI, ApoEepsilon allele frequency, and AD confirm clinical studies suggesting severe TBI to be a risk factor for the development AD higher in subjects lacking ApoEepsilon4 alleles. Further studies in larger autopsy series are needed to elucidate the relationship between TBI, genetic predisposition, and AD. SN - 1471-2377 UR - https://www.unboundmedicine.com/medline/citation/11504565/Traumatic_brain_injury_as_a_risk_factor_for_Alzheimer_disease__Comparison_of_two_retrospective_autopsy_cohorts_with_evaluation_of_ApoE_genotype_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/11504565/ DB - PRIME DP - Unbound Medicine ER -