scholarly journals Correlation between high-sensitivity C-reactive protein and brain gray matter volume in healthy elderly subjects

2012 ◽  
Vol 34 (10) ◽  
pp. 2418-2424 ◽  
Author(s):  
Yasuyuki Taki ◽  
Benjamin Thyreau ◽  
Shigeo Kinomura ◽  
Kazunori Sato ◽  
Ryoi Goto ◽  
...  
2021 ◽  
pp. 1-10
Author(s):  
Hidemasa Takao ◽  
Shiori Amemiya ◽  
Osamu Abe ◽  

Background: Scan acceleration techniques, such as parallel imaging, can reduce scan times, but reliability is essential to implement these techniques in neuroimaging. Objective: To evaluate the reproducibility of the longitudinal changes in brain morphology determined by longitudinal voxel-based morphometry (VBM) between non-accelerated and accelerated magnetic resonance images (MRI) in normal aging, mild cognitive impairment (MCI), and Alzheimer’s disease (AD). Methods: Using data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) 2 database, comprising subjects who underwent non-accelerated and accelerated structural T1-weighted MRI at screening and at a 2-year follow-up on 3.0 T Philips scanners, we examined the reproducibility of longitudinal gray matter volume changes determined by longitudinal VBM processing between non-accelerated and accelerated imaging in 50 healthy elderly subjects, 54 MCI patients, and eight AD patients. Results: The intraclass correlation coefficient (ICC) maps differed among the three groups. The mean ICC was 0.72 overall (healthy elderly, 0.63; MCI, 0.75; AD, 0.63), and the ICC was good to excellent (0.6–1.0) for 81.4%of voxels (healthy elderly, 64.8%; MCI, 85.0%; AD, 65.0%). The differences in image quality (head motion) were not significant (Kruskal–Wallis test, p = 0.18) and the within-subject standard deviations of longitudinal gray matter volume changes were similar among the groups. Conclusion: The results indicate that the reproducibility of longitudinal gray matter volume changes determined by VBM between non-accelerated and accelerated MRI is good to excellent for many regions but may vary between diseases and regions.


2004 ◽  
Vol 44 (12) ◽  
pp. 2411-2413 ◽  
Author(s):  
Christopher J.K. Hammett ◽  
Helen C. Oxenham ◽  
J. Chris Baldi ◽  
Robert N. Doughty ◽  
Rohan Ameratunga ◽  
...  

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Chi K Kim ◽  
Hyung-Min Kwon ◽  
Jong-Won Chung ◽  
Mi-Young Oh ◽  
Chang-Hun Kim ◽  
...  

Objective: Inflammatory processes are involved in the pathogenesis of atherosclerosis, and it has been known that high-sensitivity C-reactive protein (hs-CRP) is associated with coronary heart disease. However, the association of hs-CRP with subclinical cerebrovascular disease is less well established. We investigated the association of hs-CRP with silent brain infarction (SBI) as a marker of subclinical cerebrovascular disease in elderly subjects without history of overt stroke. Methods: Neurologically asymptomatic elderly subjects (n=1,443; age ≥ 65 years) who visited for routine health check-ups were included in this study. The level of hs-CRP was measured and the presence of SBI was determined by brain MRI. Results: A total of 223 subjects (15.5%) had one or more SBIs, and the average hs-CRP level was significantly higher in subjects with SBI (2.2 mg/L) than in those without (1.4 mg/L). Compared with the lowest hs-CRP group (0-0.9mg/L), the proportion of SBI in the highest hs-CRP group (≥ 3 mg/L) was increased (27.1% vs. 13.6%). After adjusting by age, gender and the history of hypertension, diabetes, smoking, hyperlipidemia and coronary heart disease, the risk of SBI was increased significantly two-fold in the highest hs-CRP group compared with the lowest group. Conclusion: Elevated hs-CRP level was found to be associated with the presence of SBI. This result suggests that inflammatory processes may be related to the subclinical cerebrovascular disease.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Akihiro Takamiya ◽  
Thomas Vande Casteele ◽  
Michel Koole ◽  
François-Laurent De Winter ◽  
Filip Bouckaert ◽  
...  

AbstractLate-life depression (LLD) is associated with a risk of developing Alzheimer’s disease (AD). However, the role of AD-pathophysiology in LLD, and its association with clinical symptoms and cognitive function are elusive. In this study, one hundred subjects underwent amyloid positron emission tomography (PET) imaging with [18F]-flutemetamol and structural MRI: 48 severely depressed elderly subjects (age 74.1 ± 7.5 years, 33 female) and 52 age-/gender-matched healthy controls (72.4 ± 6.4 years, 37 female). The Geriatric Depression Scale (GDS) and Rey Auditory Verbal Learning Test (RAVLT) were used to assess the severity of depressive symptoms and episodic memory function respectively. Amyloid deposition was quantified using the standardized uptake value ratio. Whole-brain voxel-wise comparisons of amyloid deposition and gray matter volume (GMV) between LLD and controls were performed. Multivariate analysis of covariance was conducted to investigate the association of regional differences in amyloid deposition and GMV with clinical factors, including GDS and RAVLT. As a result, there were no significant group differences in amyloid deposition. In contrast, LLD showed significant lower GMV in the left temporal and parietal region. GMV reduction in the left temporal region was associated with episodic memory dysfunction, but not with depression severity. Regional GMV reduction was not associated with amyloid deposition. LLD is associated with lower GMV in regions that overlap with AD-pathophysiology, and which are associated with episodic memory function. The lack of corresponding associations with amyloid suggests that lower GMV driven by non-amyloid pathology may play a central role in the neurobiology of LLD presenting as a psychiatric disorder.Trial registration: European Union Drug Regulating Authorities Clinical Trials identifier: EudraCT 2009-018064-95.


2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Eléna Chabran ◽  
Vincent Noblet ◽  
Paulo Loureiro de Sousa ◽  
Catherine Demuynck ◽  
Nathalie Philippi ◽  
...  

Abstract Background Fluctuations are one of the core clinical features characterizing dementia with Lewy bodies (DLB). They represent a determining factor for its diagnosis and strongly impact the quality of life of patients and their caregivers. However, the neural correlates of this complex symptom remain poorly understood. This study aimed to investigate the structural and functional changes in DLB patients, compared to Alzheimer’s disease (AD) patients and healthy elderly subjects, and their potential links with fluctuations. Methods Structural and resting-state functional MRI data were collected from 92 DLB patients, 70 AD patients, and 22 control subjects, who also underwent a detailed clinical examination including the Mayo Clinic Fluctuation Scale. Gray matter volume changes were analyzed using whole-brain voxel-based morphometry, and resting-state functional connectivity was investigated using a seed-based analysis, with regions of interest corresponding to the main nodes of the salience network (SN), frontoparietal network (FPN), dorsal attention network (DAN), and default mode network (DMN). Results At the structural level, fluctuation scores in DLB patients did not relate to the atrophy of insular, temporal, and frontal regions typically found in this pathology, but instead showed a weak correlation with more subtle volume reductions in different regions of the cholinergic system. At the functional level, the DLB group was characterized by a decreased connectivity within the SN and attentional networks, while the AD group showed decreases within the SN and DMN. In addition, higher fluctuation scores in DLB patients were correlated to a greater connectivity of the SN with the DAN and left thalamus, along with a decreased connectivity between the SN and DMN, and between the right thalamus and both the FPN and DMN. Conclusions Functional connectivity changes, rather than significant gray matter loss, could play an important role in the emergence of fluctuations in DLB. Notably, fluctuations in DLB patients appeared to be related to a disturbed external functional connectivity of the SN, which may lead to less relevant transitions between different cognitive states in response to internal and environmental stimuli. Our results also suggest that the thalamus could be a key region for the occurrence of this symptom.


Author(s):  
Valentina Pergher ◽  
Jos Tournoy ◽  
Birgitte Schoenmakers ◽  
Marc M. Van Hulle

2021 ◽  
Author(s):  
Akihiro Takamiya ◽  
Thomas Vande Casteele ◽  
Michel Koole ◽  
François-Laurent De Winter ◽  
Filip Bouckaert ◽  
...  

AbstractLate-life depression (LLD) is associated with a risk of developing Alzheimer’s disease (AD). However, the role of AD-pathophysiology in LLD, and its association with clinical symptoms and cognitive function are elusive. In this study, one hundred subjects underwent amyloid positron emission tomography (PET) imaging with [18F]-flutemetamol and structural MRI: 48 severely depressed elderly subjects (age 74.1±7.5 years, 33 female) and 52 age-/gender-matched healthy controls (72.4±6.4 years, 37 female). The Geriatric Depression Scale (GDS) and Rey Auditory Verbal Learning Test (RAVLT) were used to assess the severity of depressive symptoms and episodic memory function respectively. Amyloid deposition was quantified using the standardized uptake value ratio. Whole-brain voxel-wise comparisons of amyloid deposition and gray matter volume (GMV) between LLD and controls were performed. Multivariate analysis of covariance was conducted to investigate the association of regional differences in amyloid deposition and GMV with clinical factors, including GDS and RAVLT. As a result, there were no significant group differences in amyloid deposition. In contrast, LLD showed significant lower GMV in the left temporal and parietal region. GMV reduction in the left temporal region was associated with episodic memory dysfunction, but not with depression severity. Regional GMV reduction was not associated with amyloid deposition. LLD is associated with lower GMV in regions that overlap with AD-pathophysiology, and which are associated with episodic memory function. The lack of corresponding associations with amyloid suggests that lower GM driven by non-amyloid pathology may play a central role in the neurobiology of LLD presenting as a psychiatric disorder.


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