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Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort

BACKGROUND: Results conflict concerning the relevance of APOE alleles on the development of dementia with Lewy bodies (DLB), though they are well established in connection with Alzheimer's disease (AD). The role of APOE alleles in a Norwegian cohort of patients with DLB was therefore examined c...

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Autores principales: Berge, Guro, Sando, Sigrid B, Rongve, Arvid, Aarsland, Dag, White, Linda R
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4215279/
https://www.ncbi.nlm.nih.gov/pubmed/24639435
http://dx.doi.org/10.1136/jnnp-2013-307228
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author Berge, Guro
Sando, Sigrid B
Rongve, Arvid
Aarsland, Dag
White, Linda R
author_facet Berge, Guro
Sando, Sigrid B
Rongve, Arvid
Aarsland, Dag
White, Linda R
author_sort Berge, Guro
collection PubMed
description BACKGROUND: Results conflict concerning the relevance of APOE alleles on the development of dementia with Lewy bodies (DLB), though they are well established in connection with Alzheimer's disease (AD). The role of APOE alleles in a Norwegian cohort of patients with DLB was therefore examined compared with patients with AD and healthy control individuals. METHODS: The study included 156 patients with DLB diagnosed according to the consensus criteria guidelines, 519 patients diagnosed with AD according to the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS/ARDRA) criteria and 643 healthy elderly volunteers. Patients were recruited through hospitals, outpatient clinics, nursing homes or from local care authorities in central and south-western parts of Norway. Healthy individuals were recruited from caregivers and societies for retired people. RESULTS: Subjects carrying an APOE ε2 allele had a reduced risk for developing DLB (OR 0.4, CI 0.3 to 0.8, p=0.004), and the onset of disease was delayed by 4 years (p=0.01, Mann–Whitney U test). Conversely, the APOE ε4 allele increased the risk for development of DLB (OR 5.9, CI 2.7 to 13.0, p<0.0005 for homozygotes). Similar results were found for patients with AD regarding the effect of APOE ε2, though the protective effect appeared to be slightly less pronounced than in DLB. This study is one of the largest regarding DLB and APOE to date. CONCLUSION: The results indicate that APOE ε2, a protective factor in AD, has a clear beneficial effect on the development of DLB also.
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spelling pubmed-42152792014-11-05 Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort Berge, Guro Sando, Sigrid B Rongve, Arvid Aarsland, Dag White, Linda R J Neurol Neurosurg Psychiatry Neurodegeneration BACKGROUND: Results conflict concerning the relevance of APOE alleles on the development of dementia with Lewy bodies (DLB), though they are well established in connection with Alzheimer's disease (AD). The role of APOE alleles in a Norwegian cohort of patients with DLB was therefore examined compared with patients with AD and healthy control individuals. METHODS: The study included 156 patients with DLB diagnosed according to the consensus criteria guidelines, 519 patients diagnosed with AD according to the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS/ARDRA) criteria and 643 healthy elderly volunteers. Patients were recruited through hospitals, outpatient clinics, nursing homes or from local care authorities in central and south-western parts of Norway. Healthy individuals were recruited from caregivers and societies for retired people. RESULTS: Subjects carrying an APOE ε2 allele had a reduced risk for developing DLB (OR 0.4, CI 0.3 to 0.8, p=0.004), and the onset of disease was delayed by 4 years (p=0.01, Mann–Whitney U test). Conversely, the APOE ε4 allele increased the risk for development of DLB (OR 5.9, CI 2.7 to 13.0, p<0.0005 for homozygotes). Similar results were found for patients with AD regarding the effect of APOE ε2, though the protective effect appeared to be slightly less pronounced than in DLB. This study is one of the largest regarding DLB and APOE to date. CONCLUSION: The results indicate that APOE ε2, a protective factor in AD, has a clear beneficial effect on the development of DLB also. BMJ Publishing Group 2014-11 2014-03-17 /pmc/articles/PMC4215279/ /pubmed/24639435 http://dx.doi.org/10.1136/jnnp-2013-307228 Text en Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/
spellingShingle Neurodegeneration
Berge, Guro
Sando, Sigrid B
Rongve, Arvid
Aarsland, Dag
White, Linda R
Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort
title Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort
title_full Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort
title_fullStr Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort
title_full_unstemmed Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort
title_short Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort
title_sort apolipoprotein e ε2 genotype delays onset of dementia with lewy bodies in a norwegian cohort
topic Neurodegeneration
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4215279/
https://www.ncbi.nlm.nih.gov/pubmed/24639435
http://dx.doi.org/10.1136/jnnp-2013-307228
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