Association of Subcortical Structural Shapes With Tau, Amyloid, and Cortical Atrophy in Early-Onset and Late-Onset Alzheimer’s Disease

Lee, Eun Chong; Kang, Jae Myeong; Seo, Seongho; Seo, Ha Eun; Lee, Sang Yoon; Park, Kee Hyung; Na, Duk L.; Noh, Young; Seong, Joon Kyung

doi:10.3389/fnagi.2020.563559

Cited by 13 publications

(10 citation statements)

References 38 publications

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“…Those findings are supported by a meta-analysis and review, which also shows that mid-life obesity is related to late-life dementia [44]. previously [20,62,63]. Thus, the final distribution of phosphorylated tau extends beyond the initial site(s) of origin of the disease process.…”

Section: Correlation Between Ad and Obesity Brain Maps In Obese Ad Pa...mentioning

confidence: 62%

Obesity-Associated Neurodegeneration Pattern Mimics Alzheimer’s Disease in an Observational Cohort Study

Morys

Potvin²,

Zeighami

et al. 2023

JAD

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Background: Excess weight in adulthood leads to health complications such as diabetes, hypertension, or dyslipidemia. Recently, excess weight has also been related to brain atrophy and cognitive decline. Reports show that obesity is linked with Alzheimer’s disease (AD)-related changes, such as cerebrovascular damage or amyloid-β accumulation. However, to date no research has conducted a direct comparison between brain atrophy patterns in AD and obesity. Objective: Here, we compared patterns of brain atrophy and amyloid-β/tau protein accumulation in obesity and AD using a sample of over 1,300 individuals from four groups: AD patients, healthy controls, obese otherwise healthy individuals, and lean individuals. Methods: We age- and sex-matched all groups to the AD-patients group and created cortical thickness maps of AD and obesity. This was done by comparing AD patients with healthy controls, and obese individuals with lean individuals. We then compared the AD and obesity maps using correlation analyses and permutation-based tests that account for spatial autocorrelation. Similarly, we compared obesity and AD brain maps with amyloid-β and tau protein maps from other studies. Results: Obesity maps were highly correlated with AD maps but were not correlated with amyloid-β/tau protein maps. This effect was not accounted for by the presence of obesity in the AD group. Conclusion: Our research confirms that obesity-related grey matter atrophy resembles that of AD. Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.

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Section: Correlation Between Ad and Obesity Brain Maps In Obese Ad Pa...mentioning

confidence: 62%

Obesity-Associated Neurodegeneration Pattern Mimics Alzheimer’s Disease in an Observational Cohort Study

Morys

Potvin²,

Zeighami

et al. 2023

JAD

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“…Voxel-based MRI analysis showed no significant difference in cortical atrophy between EOAD and LOAD in our study. However, most previous ones have reported that cortical atrophy is more extensive in EOAD, although the patterns of atrophy varied 10,22,38,39 . Early-onset AD typically showed more parietal involvement, whereas LOAD was associated with more hippocampus atrophy.…”

Section: Discussionmentioning

confidence: 80%

“…6,8,9 Several studies have reported that EOAD exhibits more severe cortical atrophy, greater reduction in cerebral metabolism, and a higher degree of tau deposition than LOAD. [9][10][11][12][13][14][15] However, because of heterogeneity, heredity, and other factors, imaging features may overlap. 14,16 The impact of age at onset on Aβ deposition is controversial.…”

mentioning

confidence: 99%

Characterizing Early-Onset Alzheimer Disease Using Multiprobe PET/MRI

Xu¹,

Ruan²,

Liu³

et al. 2023

Clin Nucl Med

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PurposeEarly-onset Alzheimer disease (EOAD) is rare, highly heterogeneous, and associated with poor prognosis. This AT(N) Framework–based study aimed to compare multiprobe PET/MRI findings between EOAD and late-onset Alzheimer disease (LOAD) patients and explore potential imaging biomarkers for characterizing EOAD.MethodsPatients with AD who underwent PET/MRI in our PET center were retrospectively reviewed and grouped according to the age at disease onset: EOAD, younger than 60 years; and LOAD, 60 years or older. Clinical characteristics were recorded. All study patients had positive β-amyloid PET imaging; some patients also underwent 18F-FDG and 18F-florzolotau PET. Imaging of the EOAD and LOAD groups was compared using region-of-interest and voxel-based analysis. Correlation of onset age and regional SUV ratios were also evaluated.ResultsOne hundred thirty-three patients were analyzed (75 EOAD and 58 LOAD patients). Sex (P = 0.515) and education (P = 0.412) did not significantly differ between groups. Mini-Mental State Examination score was significantly lower in the EOAD group (14.32 ± 6.74 vs 18.67 ± 7.20, P = 0.004). β-Amyloid deposition did not significantly differ between groups. Glucose metabolism in the frontal, parietal, precuneus, temporal, occipital lobe, and supramarginal and angular gyri was significantly lower in the EOAD group (n = 49) than in the LOAD group (n = 44). In voxel-based morphometry analysis, right posterior cingulate/precuneus atrophy was more obvious in the EOAD (P < 0.001), although no voxel survived family-wise error correction. Tau deposition in the precuneus, parietal lobe, and angular, supramarginal, and right middle frontal gyri was significantly higher in the EOAD group (n = 18) than in the LOAD group (n = 13).ConclusionsMultiprobe PET/MRI showed that tau burden and neuronal damage are more severe in EOAD than in LOAD. Multiprobe PET/MRI may be useful to assess the pathologic characteristics of EOAD.

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“…Additionally, increased ventral posterolateral asymmetry in the thalamus has been noted to be associated with worse cognitive function [12]. These subcortical regions of the brain (i.e., thalamus and putamen) may be impacted earlier in AD [29], when excess Aβ production drives disease progression. One possible explanation could be that significant amyloid burden is interfering with the cortical communication pathway that goes through the subcortical regions like thalamus and putamen.…”

Section: Discussionmentioning

confidence: 99%

“…There is an ongoing question of how disease progression manifests in cortical versus subcortical brain structures [27, 28]. In a longitudinal study, researchers identified significant putamen atrophy and right dominant asymmetry as people age [29].…”

Section: Discussionmentioning

confidence: 99%

Neural asymmetry during memory encoding and its association with markers of preclinical Alzheimer’s Disease

Mizuno

et al. 2021

Preprint

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Background: Alzheimers Disease (AD) is the most common form of dementia and is characterized by cognitive dysfunction that impacts daily functioning. Beta-amyloid (Ab) is a cytotoxic protein that deposits in the brain many years prior to the onset of cognitive dysfunction. The preclinical period is a stage of AD in which significant pathology is present without clinical symptoms. Ab has been shown to deposit asymmetrically early in the AD trajectory, which has shown to have functional consequences (e.g., asymmetric hypometabolism). We aimed to investigate whether markers of AD and cognitive function were correlated with neural activation asymmetry during memory encoding tasks. Methods: We recruited participants who were cognitively normal to undergo functional magnetic resonance imaging (fMRI), positron emission tomography (PET) imaging, and cognitive testing. We conducted analyses to identify regions of significant activation during a well-established face-name pair memory encoding task, and to identify regions of significant asymmetry. We then computed hemispheric asymmetry (negative/positive values indicate left/right asymmetry, respectively) and absolute asymmetry (greater values indicate greater asymmetry in either hemisphere) and investigated their associations with age, sex, education, global cerebral amyloid, global cerebral metabolism, memory encoding task performance, white matter hyperintensities, and multiple domains of cognitive function. Results: We identified expected regions of significant activation, including the hippocampus, and identified four regions with significant left-hemisphere asymmetry: superior medial frontal gyrus, middle frontal gyrus, supplemental motor area, and medial orbitofrontal gyrus, and two regions with significant right hemisphere asymmetry: putamen and ventral posterolateral nucleus of the thalamus. We found that greater left-hemisphere asymmetry in the middle frontal gyrus was correlated with greater global cerebral glucose metabolism. We also found that better performance in memory, learning, and executive attention was associated with greater absolute symmetry in the thalamus, while better visuospatial performance was associated with greater putamen absolute symmetry. Discussion: Functional asymmetry is correlated with functional markers (e.g., glucose metabolism) in older cognitively normal adults and may reflect metabolic and cognitive changes. Longitudinal studies may help us better understand these associations and the causal impact of neural activation asymmetry.

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Association of Subcortical Structural Shapes With Tau, Amyloid, and Cortical Atrophy in Early-Onset and Late-Onset Alzheimer’s Disease

Cited by 13 publications

References 38 publications

Obesity-Associated Neurodegeneration Pattern Mimics Alzheimer’s Disease in an Observational Cohort Study

Obesity-Associated Neurodegeneration Pattern Mimics Alzheimer’s Disease in an Observational Cohort Study

Characterizing Early-Onset Alzheimer Disease Using Multiprobe PET/MRI

Neural asymmetry during memory encoding and its association with markers of preclinical Alzheimer’s Disease

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