Cargando…
Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia
BACKGROUND: We investigated the structural changes associated with Alzheimer’s disease, dementia with Lewy bodies and Parkinson disease dementia by means of cortical thickness analysis. METHODS: Two hundred and forty-five participants: 76 Alzheimer’s disease, 65 dementia with Lewy bodies, 29 Parkins...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285984/ https://www.ncbi.nlm.nih.gov/pubmed/31696728 http://dx.doi.org/10.1177/0004867419885165 |
_version_ | 1783544798184996864 |
---|---|
author | Colloby, Sean J Watson, Rosie Blamire, Andrew M O’Brien, John T Taylor, John-Paul |
author_facet | Colloby, Sean J Watson, Rosie Blamire, Andrew M O’Brien, John T Taylor, John-Paul |
author_sort | Colloby, Sean J |
collection | PubMed |
description | BACKGROUND: We investigated the structural changes associated with Alzheimer’s disease, dementia with Lewy bodies and Parkinson disease dementia by means of cortical thickness analysis. METHODS: Two hundred and forty-five participants: 76 Alzheimer’s disease, 65 dementia with Lewy bodies, 29 Parkinson disease dementia and 76 cognitively normal controls underwent 3-T T1-weighted magnetic resonance imaging and clinical and cognitive assessments. We implemented FreeSurfer to obtain cortical thickness estimates to contrast patterns of cortical thinning across groups and their clinical correlates. RESULTS: In Alzheimer’s disease and dementia with Lewy bodies, a largely similar pattern of regional cortical thinning was observed relative to controls apart from a more severe loss within the entorhinal and parahippocampal structures in Alzheimer’s disease. In Parkinson disease dementia, regional cortical thickness was indistinguishable from controls and dementia with Lewy bodies, suggesting an ‘intermediate’ pattern of regional cortical change. In terms of global cortical thickness, group profiles were controls > Parkinson disease dementia > dementia with Lewy bodies > Alzheimer’s disease (F(3, 241) ⩽ 123.2, p < 0.001), where percentage wise, the average difference compared to controls were −1.8%, −5.5% and −6.4%, respectively. In these samples, cortical thinning was also associated with cognitive decline in dementia with Lewy bodies but not in Parkinson disease dementia and Alzheimer’s disease. CONCLUSION: In a large and well-characterised cohort of people with dementia, regional cortical thinning in dementia with Lewy bodies was broadly similar to Alzheimer’s disease. There was preservation of the medial temporal lobe structures in dementia with Lewy bodies compared with Alzheimer’s disease, supporting its inclusion as a supportive biomarker in the revised clinical criteria for dementia with Lewy bodies. However, there was less global cortical thinning in Parkinson disease dementia, with no significant regional difference between Parkinson disease dementia and controls. These findings highlight the overlap across the Alzheimer’s disease/Parkinson disease dementia spectrum and the potential for differing mechanisms underlying neurodegeneration and cognition in dementia with Lewy bodies and Parkinson disease dementia. |
format | Online Article Text |
id | pubmed-7285984 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-72859842020-06-29 Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia Colloby, Sean J Watson, Rosie Blamire, Andrew M O’Brien, John T Taylor, John-Paul Aust N Z J Psychiatry Articles BACKGROUND: We investigated the structural changes associated with Alzheimer’s disease, dementia with Lewy bodies and Parkinson disease dementia by means of cortical thickness analysis. METHODS: Two hundred and forty-five participants: 76 Alzheimer’s disease, 65 dementia with Lewy bodies, 29 Parkinson disease dementia and 76 cognitively normal controls underwent 3-T T1-weighted magnetic resonance imaging and clinical and cognitive assessments. We implemented FreeSurfer to obtain cortical thickness estimates to contrast patterns of cortical thinning across groups and their clinical correlates. RESULTS: In Alzheimer’s disease and dementia with Lewy bodies, a largely similar pattern of regional cortical thinning was observed relative to controls apart from a more severe loss within the entorhinal and parahippocampal structures in Alzheimer’s disease. In Parkinson disease dementia, regional cortical thickness was indistinguishable from controls and dementia with Lewy bodies, suggesting an ‘intermediate’ pattern of regional cortical change. In terms of global cortical thickness, group profiles were controls > Parkinson disease dementia > dementia with Lewy bodies > Alzheimer’s disease (F(3, 241) ⩽ 123.2, p < 0.001), where percentage wise, the average difference compared to controls were −1.8%, −5.5% and −6.4%, respectively. In these samples, cortical thinning was also associated with cognitive decline in dementia with Lewy bodies but not in Parkinson disease dementia and Alzheimer’s disease. CONCLUSION: In a large and well-characterised cohort of people with dementia, regional cortical thinning in dementia with Lewy bodies was broadly similar to Alzheimer’s disease. There was preservation of the medial temporal lobe structures in dementia with Lewy bodies compared with Alzheimer’s disease, supporting its inclusion as a supportive biomarker in the revised clinical criteria for dementia with Lewy bodies. However, there was less global cortical thinning in Parkinson disease dementia, with no significant regional difference between Parkinson disease dementia and controls. These findings highlight the overlap across the Alzheimer’s disease/Parkinson disease dementia spectrum and the potential for differing mechanisms underlying neurodegeneration and cognition in dementia with Lewy bodies and Parkinson disease dementia. SAGE Publications 2019-11-07 2020-06 /pmc/articles/PMC7285984/ /pubmed/31696728 http://dx.doi.org/10.1177/0004867419885165 Text en © The Royal Australian and New Zealand College of Psychiatrists 2019 http://www.creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Articles Colloby, Sean J Watson, Rosie Blamire, Andrew M O’Brien, John T Taylor, John-Paul Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia |
title | Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia |
title_full | Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia |
title_fullStr | Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia |
title_full_unstemmed | Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia |
title_short | Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia |
title_sort | cortical thinning in dementia with lewy bodies and parkinson disease dementia |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285984/ https://www.ncbi.nlm.nih.gov/pubmed/31696728 http://dx.doi.org/10.1177/0004867419885165 |
work_keys_str_mv | AT collobyseanj corticalthinningindementiawithlewybodiesandparkinsondiseasedementia AT watsonrosie corticalthinningindementiawithlewybodiesandparkinsondiseasedementia AT blamireandrewm corticalthinningindementiawithlewybodiesandparkinsondiseasedementia AT obrienjohnt corticalthinningindementiawithlewybodiesandparkinsondiseasedementia AT taylorjohnpaul corticalthinningindementiawithlewybodiesandparkinsondiseasedementia |