Amyloid-β-related and unrelated cortical thinning in dementia with Lewy bodies

Lee, Young Gun; Jeon, Sohee; Yoo, Hyung Sik; Chung, Seok Jong; Lee, Seung Koo; Lee, Phil Hyu; Sohn, Young H.; Yun, Mijin; Evans, Alan C.; Ye, Byoung Seok

doi:10.1016/j.neurobiolaging.2018.08.007

Cited by 27 publications

(36 citation statements)

References 42 publications

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“…Quantitative Analyses of 18 F-FP-CIT PET 18 F-FP-CIT PET was performed using a Discovery 600 (GE Healthcare, Milwaukee, WI) device, which acquires images with a 3-dimensional resolution of 2.3-mm full-width at half-maximum. After a 6-hour fast, the patients were intravenously injected with 5 mCi (185 MBq) of 18 F-FP-CIT. At 90 minutes after the injection, PET images were acquired for 20 minutes in 3-dimensional mode at a power of 120 kVp and a current of 200 mA.…”

Section: Methods Participantsmentioning

confidence: 99%

“…At 90 minutes after the injection, PET images were acquired for 20 minutes in 3-dimensional mode at a power of 120 kVp and a current of 200 mA. 18 Image processing was performed using MATLAB (The MathWorks, Inc, Natick, MA) software for statistical parametric mapping 8 (http://www.fil.ion/uc.ac.uk/ spm) and ITK-SNAP (http://www.itksnap.org). All reconstructed 18 F-FP-CIT images were normalized to the 18 F-FP-CIT template, which was made using the 18 F-FP-CIT PET images and T1-weighted magnetic resonance images of 40 healthy controls, as described previously.…”

Section: Methods Participantsmentioning

confidence: 99%

“…18 Image processing was performed using MATLAB (The MathWorks, Inc, Natick, MA) software for statistical parametric mapping 8 (http://www.fil.ion/uc.ac.uk/ spm) and ITK-SNAP (http://www.itksnap.org). All reconstructed 18 F-FP-CIT images were normalized to the 18 F-FP-CIT template, which was made using the 18 F-FP-CIT PET images and T1-weighted magnetic resonance images of 40 healthy controls, as described previously. 19 Briefly, all of the healthy controls from which the 18 F-FP-CIT template was derived had no previous history of neurologic or psychiatric illness.…”

Section: Methods Participantsmentioning

confidence: 99%

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Identifying the Functional Brain Network of Motor Reserve in Early Parkinson's Disease

et al. 2020

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A BS TRACT: Background: The severity of motor symptoms in Parkinson's disease (PD) does not always correlate with the degree of nigral dopaminergic neuronal loss. Individuals with greater motor reserve may have milder motor signs than their striatal dopamine loss. In this study, we explored the functional brain network associated with motor reserve in early-stage PD. Methods: We analyzed 134 patients with de novo PD who underwent dopamine transporter scans and restingstate functional magnetic resonance imaging. We estimated individual motor reserve based on initial motor deficits and striatal dopamine depletion using a residual model. We applied network-based statistic analysis to identify the functional brain network associated with the measure of motor reserve (ie, motor reserve network). We also assessed the effect of motor reserve network connectivity strength on the longitudinal increase in levodopa-equivalent dose during the 2-year follow-up period. Results: Network-based statistic analysis identified the motor reserve network composed of the basal ganglia, inferior frontal cortex, insula, and cerebellar vermis at a primary threshold of P value 0.001. Patients with an increased degree of functional connectivity within the motor reserve network had greater motor reserve. There was a significant interaction between the motor reserve network strength and time in the linear mixed model, indicating that higher motor reserve network strength was associated with slower longitudinal increase in levodopa-equivalent dose. Conclusions: The present study revealed the functional brain network associated with motor reserve in patients with early-stage PD. Functional connections within the motor reserve network are associated with the individual's capacity to cope with PD-related pathologies.

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Section: Methods Participantsmentioning

confidence: 99%

Section: Methods Participantsmentioning

confidence: 99%

Section: Methods Participantsmentioning

confidence: 99%

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Identifying the Functional Brain Network of Motor Reserve in Early Parkinson's Disease

et al. 2020

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“…Detailed methods for FP‐CIT‐PET and FBB PET acquisitions have been described in a previous study (Y. G. Lee, Jeon, et al., 2018). On the basis of visual ratings by an expert reader (M.Y.)…”

Section: Methodsmentioning

confidence: 99%

Structural connectivity networks in Alzheimer’s disease and Lewy body disease

et al. 2021

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Objective We evaluated disruption of the white matter (WM) network related with Alzheimer's disease (AD) and Lewy body disease (LBD), which includes Parkinson's disease and dementia with Lewy bodies. Methods We consecutively recruited 37 controls and 77 patients with AD‐related cognitive impairment (ADCI) and/or LBD‐related cognitive impairment (LBCI). Diagnoses of ADCI and LBCI were supported by amyloid PET and dopamine transporter PET, respectively. There were 22 patients with ADCI, 19 patients with LBCI, and 36 patients with mixed ADCI/LBCI. We investigated the relationship between ADCI, LBCI, graph theory‐based network measures on diffusion tensor images, and cognitive dysfunction using general linear models after controlling for age, sex, education, deep WM hyperintensities (WMH), periventricular WMH, and intracranial volume. Results LBCI, especially mixed with ADCI, was associated with increased normalized path length and decreased normalized global efficiency. LBCI was related to the decreased nodal degree of left caudate, which was further associated with broad cognitive dysfunction. Decreased left caudate nodal degree was associated with decreased fractional anisotropy (FA) in the brain regions vulnerable to LBD. Compared with the control group, the LBCI group had an increased betweenness centrality in the occipital nodes, which was associated with decreased FA in the WM adjacent to the striatum and visuospatial dysfunction. Conclusion Concomitant ADCI and LBCI are associated with the accentuation of LBCI‐related WM network disruption centered in the left caudate nucleus. The increase of occipital betweenness centrality could be a characteristic biologic change associated with visuospatial dysfunction in LBCI.

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“…Finally, we extracted the global FBB SUVR value as the cortical volume-weighted average of the following cortical regions of interest: frontal, anterior/posterior cingulate, lateral parietal, and lateral temporal cortices. FP-CIT-PET was interpreted using visual ratings as previously described [33]. FBB-PET was regarded as amyloid-positive if the global FBB SUVR was >1.478, as described in a previous autopsy-validation study [20].…”

Section: Apoe Genotypingmentioning

confidence: 99%

Apolipoprotein E4, amyloid, and cognition in Alzheimer's and Lewy body disease

Jung

Jeon

Baik

et al. 2021

Neurobiology of Aging

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Background: The role of APOE4 in the risk of Alzheimer's disease, Lewy body disease, and their mixed diseases have not been evaluated in antemortem patients. Also, the APOE4 effect on β-amyloid deposition and cognition, with consideration of both Alzheimer's and Lewy body diseases, remains unclear. We aimed to determine the APOE4 effects on the risk of Alzheimer's disease, Lewy body disease, and their mixed diseases, as well as on β-amyloid deposition and cognition after adjusting for the effect of Alzheimer's disease and Lewy body disease.Methods: Based on clinical features and 18 F-Florbetaben and dopamine transporter PET, we recruited 126 controls, 90 patients with typical Alzheimer's disease (57 pure Alzheimer's disease, 32 Lewy body variant of Alzheimer's disease), 77 with typical Lewy body disease (56 pure Lewy body disease, 21 dementia with Lewy bodies with amyloid deposition), and 42 with typical Alzheimer's disease/dementia with Lewy bodies. We used logistic regression analysis to investigate the effect of APOE4 on the risk of each disease and general linear models to investigate the independent and interaction effects of APOE4, Alzheimer's disease, and Lewy body disease on β-amyloid deposition and cognition.Results: APOE4 was associated with increased risks of all disease subtypes except pure Lewy body disease. APOE4 was associated with increased frontal β-amyloid burden, typical Alzheimer's disease was associated with increased β-amyloid burden in all lobar regions, and typical Lewy body disease interacted with APOE4 to increase the occipital β-amyloid burden. The interaction of APOE4 and typical Alzheimer's disease was associated with more severe memory dysfunction, while that of APOE4 and typical Lewy body disease was associated with poorer Clinical Dementia Rating Sum of Boxes.Conclusions: Our ndings suggest that the APOE4 effect on disease risk is dependent on β-amyloid deposition and APOE4 is associated with β-amyloid deposition regardless of the clinical diagnosis; however, APOE4 further interacts with typical Lewy body disease to induce worse general cognition and higher occipital β-amyloid deposition and it interacts with typical Alzheimer's disease to decrease memory function. This study highlights the possible interaction of β-amyloid and Lewy body pathologies converging in the occipital cortex through the APOE4 effect.

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Amyloid-β-related and unrelated cortical thinning in dementia with Lewy bodies

Cited by 27 publications

References 42 publications

Identifying the Functional Brain Network of Motor Reserve in Early Parkinson's Disease

Identifying the Functional Brain Network of Motor Reserve in Early Parkinson's Disease

Structural connectivity networks in Alzheimer’s disease and Lewy body disease

Apolipoprotein E4, amyloid, and cognition in Alzheimer's and Lewy body disease

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