ENHANCEMENT OF SPLENIC GLUCOSE METABOLISM DURING ACUTE MALARIAL INFECTION: CORRELATION OF FINDINGS OF FDG-PET IMAGING WITH PATHOLOGICAL CHANGES IN A PRIMATE MODEL OF SEVERE HUMAN MALARIA

2006 ◽  
Vol 74 (3) ◽  
pp. 353-360 ◽  
Author(s):  
SATORU KAWAI ◽  
TETSUYA HIGUCHI ◽  
JUN MATSUMOTO ◽  
HARUYASU YAMAGUCHI ◽  
TOMIO INOUE ◽  
...  
2021 ◽  
Vol 18 ◽  
Author(s):  
Amir Ashraf-Ganjouei ◽  
Kamyar Moradi ◽  
Shahriar Faghani ◽  
AmirHussein Abdolalizadeh ◽  
Mohammadreza Khomeijani-Farahani ◽  
...  

Background: Mild cognitive impairment (MCI) is a state between normal cognition and dementia. However, MCI diagnosis does not necessarily guarantee the progression to dementia. Since no previous study investigated brain positron emission tomography (PET) imaging of MCI-- to-normal reversion, we provided PET imaging of MCI-to-normal reversion using the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Methods: We applied comprehensive neuropsychological criteria (NP criteria), consisting of mem- ory, language, and attention/executive function domains, to include patients with a baseline diagno- sis of MCI (n=613). According to the criteria, the year 1 status of the patients was categorized into three groups (reversion: n=105, stable MCI: n=422, conversion: n=86). Demographic, neuropsycho- logical, genetic, CSF, and cognition biomarker variables were compared between the groups. Addi- tionally, after adjustment for confounding variables, the deposition pattern of amyloid-β and cere- bral glucose metabolism were compared between three groups via AV45- and FDG-PET modali- ties, respectively. Results: MCI reversion rate was 17.1% during one year of follow-up. The reversion group had the lowest frequency of APOE ε4+ subjects, the highest CSF level of amyloid-β, and the lowest CSF levels of t-tau and p-tau. Neuropsychological assessments were also suggestive of better cognitive performance in the reversion group. Patients with reversion to normal state had higher glucose metabolism in bilateral angular and left middle/inferior temporal gyri, when compared to those with stable MCI state. Meanwhile, lower amyloid-β deposition at baseline was observed in the fron- tal and parietal regions of the reverted subjects. On the other hand, the conversion group showed lower cerebral glucose metabolism in bilateral angular and bilateral middle/inferior temporal gyri compared to the stable MCI group, whereas the amyloid-β accumulation was similar between the groups. Conclusions: This longitudinal study provides novel insight regarding the application of PET imag- ing in predicting MCI transition over time.


2013 ◽  
Vol 106 ◽  
pp. S107
Author(s):  
A. Roszak ◽  
B. Urbanski ◽  
E. Burchardt ◽  
J. Kazmierska ◽  
Z. Warenczak-Florczak ◽  
...  

2018 ◽  
Vol 01 (01) ◽  
pp. 27-31 ◽  
Author(s):  
Haibo Tan ◽  
Xiuming Li ◽  
Kai Wei ◽  
Yihui Guan

Aim: To assess the changes of brain glucose metabolism and abnormal intracerebral loop in early Parkinson’s disease (PD) patients with visual spatial dysfunction by [Formula: see text]F-fluorodeoxyglucose ([Formula: see text]F-FDG) positron emission tomography (PET) imaging. Materials and Methods: This study includes three groups: early PD patients with visual spatial dysfunction ([Formula: see text]), early PD patients without visual spatial dysfunction ([Formula: see text]) and healthy controls ([Formula: see text]). Resting-state [Formula: see text]F-FDG PET was performed to obtain the imaging of brain glucose metabolism. Statistical Parametric Mapping (SPM) was used for data analyses to compare the brain glucose metabolic changes among different groups. Results: Compared with the healthy controls, early PD patients (with/without visual spatial dysfunction) showed hypermetabolism in putamen, globus pallidus, thalamus, pons, cerebellum and primary motor cortex, and hypometabolism in part of the occipital and temporal lobes. Compared with early PD patients without visual spatial dysfunction, those with visual spatial dysfunction further showed hypometabolism in visual regions including bilateral lateral prefrontal cortices and posterior parietal lobules, besides occipital and temporal lobes. Conclusion: The occurrence of abnormal glucose metabolism in the brain visual processing areas was closely associated with visual spatial dysfunction in PD patients.


PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0260482
Author(s):  
Ina Jahreis ◽  
Pablo Bascuñana ◽  
Tobias L. Ross ◽  
Jens P. Bankstahl ◽  
Marion Bankstahl

Purpose Alterations in brain glucose metabolism detected by 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) positron emission tomography (PET) may serve as an early predictive biomarker and treatment target for epileptogenesis. Here, we aimed to investigate changes in cerebral glucose metabolism before induction of epileptogenesis, during epileptogenesis as well as during chronic epilepsy. As anesthesia is usually unavoidable for preclinical PET imaging and influences the distribution of the radiotracer, four different protocols were compared. Procedures We investigated 18F-FDG uptake phase in conscious rats followed by a static scan as well as dynamic scans under continuous isoflurane, medetomidine-midazolam-fentanyl (MMF), or propofol anesthesia. Furthermore, we applied different analysis approaches: atlas-based regional analysis, statistical parametric mapping, and kinetic analysis. Results At baseline and compared to uptake in conscious rats, isoflurane and propofol anesthesia resulted in decreased cortical 18F-FDG uptake while MMF anesthesia led to a globally decreased tracer uptake. During epileptogenesis, MMF anesthesia was clearly best distinctive for visualization of prominently increased glucometabolism in epilepsy-related brain areas. Kinetic modeling further increased sensitivity, particularly for continuous isoflurane anesthesia. During chronic epilepsy, hypometabolism affecting more or less the whole brain was detectable with all protocols. Conclusion This study reveals evaluation of anesthesia protocols for preclinical 18F-FDG PET imaging as a critical step in the study design. Together with an appropriate data analysis workflow, the chosen anesthesia protocol may uncover otherwise concealed disease-associated regional glucometabolic changes.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Andrew C Ha ◽  
Jennifer Renaud ◽  
Stephanie Thorn ◽  
Rob deKemp ◽  
Keiichiro Yoshinaga ◽  
...  

Background : The PRKAG2 gene encodes for the gamma-2 subunit of AMP-activated protein kinase (AMPK), a protein implicated in the regulation of myocardial glucose metabolism. In humans, mutations of the PRKAG2 gene result in a cardiomyopathy characterized by ventricular pre-excitation, atrioventricular conduction disease, and cardiac hypertrophy. It is recognized that altered cardiac glucose metabolism and abnormal glycogen stores are responsible for the clinical manifestations of this syndrome. Since myocardial glucose uptake can be measured with 2-[ 18 F]Fluoro-2-deoxyglucose dynamic positron emission tomography ([ 18 F]FDG PET), we examined whether adult patients with an identified Arg302Gln PRKAG2 mutation have altered myocardial glucose uptake using this imaging modality. Methods: [ 18 F]FDG PET was performed in 5 adult patients with the Arg302Gln PRKAG2 mutation (PRKAG2) and in 6 healthy volunteers (Control) with a hyperinsulinemic euglycemic clamp protocol. The fractional rate of radiotracer uptake (K) is derived from PATLAK analysis. The rate of myocardial glucose uptake (rMGU) of the left ventricle (LV) is calculated as (K / LC) x P glucose , where P glucose represents the mean plasma glucose level during imaging. LC (lump constant) corrects for the differences in the transport and phosphorylation of [ 18 F]FDG and glucose. Results are expressed as mean ± standard deviation and are analyzed with the student t-test. Results: The mean rMGU in the PRKAG2 group was significantly lower than the control group. There was no difference in the mean plasma glucose levels between the 2 groups. (Table ) Conclusion: Myocardial glucose uptake is reduced in adult patients with mutation of the PRKAG2 gene when compared to normal controls. Measurement of rMGU using [ 18 F]FDG PET imaging appears to be a useful tool to investigate the pathophysiology of the PRKAG2 cardiac syndrome and to potentially distinguish this metabolic cardiomyopathy from other etiolgies. Mean rate of myocardial glucose uptake between patients with the PRKAG2 mutation and normal controls


GeroScience ◽  
2020 ◽  
Author(s):  
Marco Canevelli ◽  
◽  
Ivan Arisi ◽  
Ilaria Bacigalupo ◽  
Andrea Arighi ◽  
...  

AbstractThe present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF Aβ1-42, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of Aβ1-42, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes.


Neuroscience ◽  
2019 ◽  
Vol 417 ◽  
pp. 35-44 ◽  
Author(s):  
Jingjing Su ◽  
Qi Huang ◽  
Shuhua Ren ◽  
Fang Xie ◽  
Yu Zhai ◽  
...  

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