Topography of cortical thinning in the Lewy body diseases

Ye, Rong; Touroutoglou, Alexandra; Brickhouse, Michael; Katz, Samantha; Growdon, John H.; Johnson, Keith A.; Dickerson, Bradford C.; Gomperts, Stephen N.

doi:10.1016/j.nicl.2020.102196

Cited by 18 publications

(22 citation statements)

References 57 publications

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“…Comparisons between DLB and PDD have revealed substantial variability, with DLB generally reported to have greater cortical degeneration but inconsistent localization of atrophy. 13,14 Only rare in vivo studies have directly investigated the impact of AD co-pathology on the extent of cortical atrophy in LBD, 4,15,16 mostly using ordinal ratings of autopsy data for group-wise comparisons. Recent advances in digital histopathology provide the ability to acquire more fine-grained quantification of pathology necessary for detailed regional analyses.…”

Section: Introductionmentioning

confidence: 99%

“…Several studies also showed less severe cortical atrophy in DLB relative to Alzheimer’s disease (AD) 3,4,11,12 ; however prominent cortical atrophy does not exclude a diagnosis of DLB or PD. Comparisons between DLB and PDD have revealed substantial variability, with DLB generally reported to have greater cortical degeneration but inconsistent localization of atrophy 13,14 . Only rare in vivo studies have directly investigated the impact of AD co‐pathology on the extent of cortical atrophy in LBD, 4,15,16 mostly using ordinal ratings of autopsy data for group‐wise comparisons.…”

Section: Introductionmentioning

confidence: 99%

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Tau pathology associates with in vivo cortical thinning in Lewy body disorders

Spotorno

Coughlin

Olm

et al. 2020

Ann Clin Transl Neurol

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Objectives: To investigate the impact of Alzheimer's disease (AD) co-pathology on an in vivo structural measure of neurodegeneration in Lewy body disorders (LBD). Methods: We studied 72 LBD patients (Parkinson disease (PD) = 2, PD-MCI = 25, PD with dementia = 10, dementia with Lewy bodies = 35) with either CSF analysis or neuropathological examination and structural MRI during life. The cohort was divided into those harboring significant AD co-pathology, either at autopsy (intermediate/high AD neuropathologic change) or with CSF signature indicating AD co-pathology (t-tau/Ab 1-42 > 0.3) (LBD+AD, N = 19), and those without AD co-pathology (LBDÀAD, N = 53). We also included a reference group of 25 patients with CSF biomarker-confirmed amnestic AD. We investigated differences in MRI cortical thickness estimates between groups, and in the 21 autopsied LBD patients (LBDÀAD = 14, LBD+AD = 7), directly tested the association between antemortem MRI and post-mortem burdens of tau, Ab, and alpha-synuclein using digital histopathology in five representative neocortical regions. Results: The LBD+AD group was characterized by cortical thinning in anterior/medial and lateral temporal regions (P < 0.05 FWE-corrected) relative to LBDÀAD. In LBD+AD, cortical thinning was most pronounced in temporal neocortex, whereas the AD reference group showed atrophy that equally encompassed temporal, parietal and frontal neocortex. In autopsied LBD, we found an inverse correlation with cortical thickness and post-mortem tau pathology, while cortical thickness was not significantly associated with Ab or alpha-synuclein pathology. Interpretation: LBD+AD is characterized by temporal neocortical thinning on MRI, and cortical thinning directly correlated with post-mortem histopathologic burden of tau, suggesting that tau pathology influences the pattern of neurodegeneration in LBD.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Tau pathology associates with in vivo cortical thinning in Lewy body disorders

Spotorno

Coughlin

Olm

et al. 2020

Ann Clin Transl Neurol

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“…Whether the use of cognitive-enhancing medications was masking any significant difference in the severity of cognitive impairment or any other clinical scales between the two groups remains uncertain and needs to be explored in future studies. Previous PET studies in DLB have not identified any associations between Aβ load and clinical features; only one study (Donaghy et al, 2018) reported the frequencies of cognitive-enhancing medication use, which were similar between Aβ+ and Aβ− DLB (Donaghy et al, 2018;Lee et al, 2018;Ye et al, 2020). Even in people with AD, studies have shown that tau pathology, not Aβ, had the strongest negative influence on cognition and disease trajectory (Aschenbrenner et al, 2018;Pontecorvo et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Association between amyloid-beta deposition and cortical thickness in dementia with Lewy bodies

Chin

Gajamange

Desmond

et al. 2022

Aust N Z J Psychiatry

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Objective: Amyloid-beta often co-exists in dementia with Lewy bodies, but its clinical relevance in dementia with Lewy bodies remains unclear. This study aimed to investigate the clinical and imaging correlates of amyloid-beta deposition in dementia with Lewy bodies, particularly its relationship with cortical thickness in Alzheimer’s disease–prone regions and hippocampal volume. Methods: Twenty-four participants with probable dementia with Lewy bodies underwent high-resolution magnetic resonance imaging and amyloid-beta positron emission tomography imaging using the radiotracer 18F-NAV4694. Amyloid-beta deposition was quantified and reported using the Centiloid method. Results: Amyloid-beta positivity, defined as Centiloid > 50, was present in 45.8% of dementia with Lewy bodies participants. There were no statistically significant differences in clinical characteristics between Aβ+ and Aβ− dementia with Lewy bodies. Compared with the Aβ− group, Aβ+ dementia with Lewy bodies exhibited greater global cortical thinning as well as in the Alzheimer’s disease–prone region of interest, adjusted for age, sex and years of education. A mean cortical thickness of 5.12 mm across a combined meta-region of interest has a sensitivity of 88.9% and specificity of 90.0% in discriminating Aβ+ from Aβ− dementia with Lewy bodies. Hippocampal volume was not different between groups. Conclusion: Early structural changes in cortical thickness, but not hippocampal volume, were observed in dementia with Lewy bodies with significant amyloid-beta burden. This may represent an early Alzheimer’s disease–related neurodegenerative process.

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“…Prior research has suggested that cognitive impairment most often results from neurodegenerative diseases such as AD [ 34 ], as well as other related disorders such as frontotemporal lobular degeneration (FTD) [ 35 ], progressive supranuclear palsy (PSP) [ 36 ], Parkinson’s disease (PD) [ 37 ], dementia with Lewy bodies (DLB) [ 38 ], and amyotrophic lateral sclerosis (ALS) [ 39 ]. These studies suggest that the areas identified in the derived WTC-CI signature may have identified regions active across a range of neurodegenerative conditions including, for example, regions within the temporal lobe that are commonly implicated in AD with focal points in the medial temporal, inferior temporal, temporal pole as well as subregions of the frontal lobe, the right parietal lobe as seen in PD, and the left frontal lobe and supramarginal regions as seen in PSP.…”

Section: Discussionmentioning

confidence: 99%