Cortical Thickness in Dementia with Lewy Bodies and Alzheimer's Disease: A Comparison of Prodromal and Dementia Stages

Abstract

Objectives: To assess and compare cortical thickness (CTh) of patients with prodromal Dementia with Lewy bodies (pro-DLB), prodromal Alzheimer's disease (pro-AD), DLB dementia (DLB-d), AD dementia (AD-d) and normal ageing.

Methods: Study participants(28 pro-DLB, 27 pro-AD, 31 DLB-d, 54 AD-d and 33 elderly controls) underwent 3Tesla T1 3D MRI and detailed clinical and cognitive assessments. We used FreeSurfer analysis package to measure CTh and investigate patterns of cortical thinning across groups.

Results: Comparison of CTh between pro-DLB and pro-AD (p<0.05, FDR corrected) showed more right anterior insula thinning in pro-DLB, and more bilateral parietal lobe and left parahippocampal gyri thinning in pro-AD. Comparison of prodromal patients to healthy elderly controls showed the involvement of the same regions. In DLB-d (p<0.05, FDR corrected) cortical thinning was found predominantly in the right temporo-parietal junction, and insula, cingulate, orbitofrontal and lateral occipital cortices. In AD-d(p<0.05, FDR corrected),the most significant areas affected included the entorhinal cortices, parahippocampal gyri and parietal lobes. The comparison of AD-d and DLB-d demonstrated more CTh in AD-d in the left entorhinal cortex (p<0.05, FDR corrected).

Conclusion: Cortical thickness is a sensitive measure for characterising patterns of grey matter atrophy in early stages of DLB distinct from AD. Right anterior insula involvement may be a key region at the prodromal stage of DLB and needs further investigation.

Fig 1. Flow Chart of the present study on cortical thickness in prodromal and dementia stages of Lewy body dementia and Alzheimer's disease.

AD = Alzheimer’s disease; DLB = Dementia with Lewy bodies; MCI = Mild Cognitive Impairment. Prodromal DLB means patients with McKeith's criteria of DLB with cognitive impairment but without dementia. Psychiatric pathologies included two patients with depression, one with bipolar disorder, and one histrionic personality disorder; and one cognitive impairment due to severe sleep apnoea, one vitamin B12 encephalopathy, and one mitochondriopathy for patients with MCI. Other brain pathologies included one Parkinson's disease dementia, one DLB with primary Sjögren's syndrome, one with chronic brain autoimmune encephalitis and one dementia without evolution for more than 10 years, for patients with dementia

Fig 2. Cortical thinning patterns in pro-DLB, pro-AD, DLB-d and AD-d compared to healthy older controls (A = Anterior, P = Posterior, FDR = False Discovery Rate).

Fig 3. Patterns of Cortical thinning between Pro-AD and Pro-DLB and between AD-d and DLB-d (A = Anterior, P = Posterior, FDR = False Discovery Rate).

Fig 4. Correlations between cortical thickness and MMSE for dementia with Lewy bodies (pro-DLB and DLB-d: DLB) and Alzheimer's disease (pro-AD and AD-d: AD) patients (A = Anterior, P = Posterior, FDR = False Discovery Rate).