scholarly journals Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia

2019 ◽  
Vol 54 (6) ◽  
pp. 633-643
Author(s):  
Sean J Colloby ◽  
Rosie Watson ◽  
Andrew M Blamire ◽  
John T O’Brien ◽  
John-Paul Taylor

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 (F3, 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.

2010 ◽  
Vol 21 (4) ◽  
pp. 1129-1140 ◽  
Author(s):  
Michael J. Firbank ◽  
Andrew M. Blamire ◽  
Andrew Teodorczuk ◽  
Emma Teper ◽  
Emma J. Burton ◽  
...  

2016 ◽  
Vol 31 (9) ◽  
pp. 1075-1083 ◽  
Author(s):  
Ellen Svendsboe ◽  
Toril Terum ◽  
Ingelin Testad ◽  
Dag Aarsland ◽  
Ingun Ulstein ◽  
...  

2015 ◽  
Vol 36 (4) ◽  
pp. 1743-1750 ◽  
Author(s):  
Elijah Mak ◽  
Li Su ◽  
Guy B. Williams ◽  
Rosie Watson ◽  
Michael J. Firbank ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Markus Donix ◽  
Maria Scharf ◽  
Kira Marschner ◽  
Annett Werner ◽  
Cathrin Sauer ◽  
...  

Cardiovascular risk factors influence onset and progression of Alzheimer’s disease. Among cognitively healthy people, changes in brain structure and function associated with high blood pressure, diabetes, or other vascular risks suggest differential regional susceptibility to neuronal damage. In patients with Alzheimer’s disease, hippocampal and medial temporal lobe atrophy indicate early neuronal loss preferentially in key areas for learning and memory. We wanted to investigate whether this regional cortical thinning would be modulated by cardiovascular risk factors. We utilized high-resolution magnetic resonance imaging and a cortical unfolding technique to determine the cortical thickness of medial temporal subregions in 30 patients with Alzheimer’s disease. Cardiovascular risk was assessed using a sex-specific multivariable risk score. Greater cardiovascular risk was associated with cortical thinning in the hippocampus CA2/3/dentate gyrus area but not other hippocampal and medial temporal subregions. APOE genotype, a family history of Alzheimer’s disease, and age did not influence cortical thickness. Alzheimer’s disease-related atrophy could mask the influence of genetic risk factors or age on regional cortical thickness in medial temporal lobe regions, whereas the impact of vascular risk factors remains detectable. This highlights the importance of cardiovascular disease prevention and treatment in patients with Alzheimer’s disease.


PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0127396 ◽  
Author(s):  
Frederic Blanc ◽  
Sean J. Colloby ◽  
Nathalie Philippi ◽  
Xavier de Pétigny ◽  
Barbara Jung ◽  
...  

2014 ◽  
Vol 10 ◽  
pp. P111-P111
Author(s):  
Rosie Watson ◽  
Sean J. Colloby ◽  
Andrew Blamire ◽  
John O'Brien

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