Subcortical volume changes in dementia with Lewy bodies and Alzheimer’s disease
The April International Psychogeriatrics Article of the Month is entitled “Subcortical volume changes in dementia with Lewy bodies and Alzheimer’s disease. A comparison with healthy aging” by Rosie Watson, Sean J. Colloby, Andrew M. Blamire and John T. O’Brien.
This post is authored by Rosie Watson and Sean Colloby
Subcortical volume changes in dementia with Lewy bodies and Alzheimer’s disease. A comparison with healthy aging.
Dementia with Lewy bodies (DLB) and Alzheimer’s disease (AD) are the leading causes of dementia in older age. It can be difficult to accurately diagnose DLB as some of the symptoms are similar to those experienced by people with AD, particularly as the disease progresses and people with DLB are often misdiagnosed as having AD during life. The importance of diagnostic accuracy is clear – it is needed to access appropriate information and treatment and avoid treatments that may worsen the condition (e.g. antipsychotic medication can cause potentially fatal sensitivity reactions in DLB).
We have previously reported the patterns of cortical atrophy in this cohort – greater cortical grey matter volume loss in AD when compared to DLB, despite similar levels of dementia severity. Furthermore, post-mortem studies have indicated that the deep brain subcortical structures (see figure) are vulnerable to Lewy body related pathology, also consistent with the symptoms people with DLB experience. The development of sophisticated techniques to analyse brain imaging data has enabled us to assess the subcortical structures during life.
One hundred older participants (33 DLB, 32 AD and 35 healthy controls) underwent MRI brain scanning. We found greater volume loss in the brainstem in DLB when compared with controls that was not apparent in AD. Furthermore, the total subcortical grey matter volume measure for AD and DLB was significantly lower than in the control group and appeared to be more marked in DLB. Given the relatively low cortical grey matter volume loss in DLB compared with AD, it may indicate that change occurs in the subcortical structures at an earlier stage of the disease course in this condition.
The lack of significant differences between AD and DLB may reflect low statistical power due to known disease heterogeneity and the fact that differing disease pathologies do not evolve at the same rate. However, the suggestion of greater change in the subcortical structures in DLB highlights the importance of these structures in this disease. Further work is required to understand the neurobiological role and potential for development of disease markers to better separate the conditions clinically.