Appetitive Regulation in Anorexia Nervosa and Bulimia Nervosa

Author(s):  
Walter Kaye ◽  
Alice V. Ely

Anorexia and bulimia nervosa are complex disorders with dysregulated appetitive behaviors. The underlying causes of disturbed patterns of eating are unknown, but a growing body of research suggests that aberrant functioning of brain or peripheral systems may be responsible. Neuroimaging technologies, such as positron emission tomography (PET) and functional MRI (fMRI), can be used to explore whether there are perturbations of the monoamine systems, the neurocircuitry of gustatory processing in eating disorders, and their relationship to metabolic homeostatic states. Together, PET and fMRI data suggest that individuals with eating disorders have disturbance of taste- and reward-processing regions of the brain, which may contribute to eating disorder symptoms.

Author(s):  
Walter Kaye ◽  
Tyson Oberndorfer

Anorexia and bulimia nervosa are complex disorders with dysregulated appetitive behaviors. The underlying causes of disturbed eating patterns are unknown, but in theory, could involve aberrant functioning of brain or peripheral systems. New technologies, such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), can be used to explore whether there are perturbations of the monoamine systems and the neurocircuitry of gustatory processing in eating disorders. Together, PET and fMRI data suggest that individuals with eating disorders have disturbance of taste and reward processing regions of the brain, which may contribute to eating disorder symptoms.


2021 ◽  
Vol 22 (15) ◽  
pp. 8051
Author(s):  
Rodrigo Teodoro ◽  
Daniel Gündel ◽  
Winnie Deuther-Conrad ◽  
Lea Ueberham ◽  
Magali Toussaint ◽  
...  

Cannabinoid receptors type 2 (CB2R) represent an attractive therapeutic target for neurodegenerative diseases and cancer. Aiming at the development of a positron emission tomography (PET) radiotracer to monitor receptor density and/or occupancy during a CB2R-tailored therapy, we herein describe the radiosynthesis of cis-[18F]1-(4-fluorobutyl-N-((1s,4s)-4-methylcyclohexyl)-2-oxo-1,2-dihydro-1,8-naphthyridine-3-carboxamide ([18F]LU14) starting from the corresponding mesylate precursor. The first biological evaluation revealed that [18F]LU14 is a highly affine CB2R radioligand with >80% intact tracer in the brain at 30 min p.i. Its further evaluation by PET in a well-established rat model of CB2R overexpression demonstrated its ability to selectively image the CB2R in the brain and its potential as a tracer to further investigate disease-related changes in CB2R expression.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Si Eun Kim ◽  
Byungju Lee ◽  
Hyemin Jang ◽  
Juhee Chin ◽  
Ching Soong Khoo ◽  
...  

Abstract Background The presence of ß-amyloid (Aß) in the brain can be identified using amyloid PET. In clinical practice, the amyloid PET is interpreted based on dichotomous visual rating, which renders focal Aß accumulation be read as positive for Aß. However, the prognosis of patients with focal Aß deposition is not well established. Thus, we investigated cognitive trajectories of patients with focal Aß deposition. Methods We followed up 240 participants (112 cognitively unimpaired [CU], 78 amnestic mild cognitive impairment [aMCI], and 50 Alzheimer’s disease (AD) dementia [ADD]) for 2 years from 9 referral centers in South Korea. Participants were assessed with neuropsychological tests and 18F-flutemetamol (FMM) positron emission tomography (PET). Ten regions (frontal, precuneus/posterior cingulate (PPC), lateral temporal, parietal, and striatum of each hemisphere) were visually examined in the FMM scan, and participants were divided into three groups: No-FMM, Focal-FMM (FMM uptake in 1–9 regions), and Diffuse-FMM. We used mixed-effects model to investigate the speed of cognitive decline in the Focal-FMM group according to the cognitive level, extent, and location of Aß involvement, in comparison with the No- or Diffuse-FMM group. Results Forty-five of 240 (18.8%) individuals were categorized as Focal-FMM. The rate of cognitive decline in the Focal-FMM group was faster than the No-FMM group (especially in the CU and aMCI stage) and slower than the Diffuse-FMM group (in particular in the CU stage). Within the Focal-FMM group, participants with FMM uptake to a larger extent (7–9 regions) showed faster cognitive decline compared to those with uptake to a smaller extent (1–3 or 4–6 regions). The Focal-FMM group was found to have faster cognitive decline in comparison with the No-FMM when there was uptake in the PPC, striatum, and frontal cortex. Conclusions When predicting cognitive decline of patients with focal Aß deposition, the patients’ cognitive level, extent, and location of the focal involvement are important.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yu Liu ◽  
Lizhen Wang ◽  
Donghui Pan ◽  
Mingzhu Li ◽  
Yaoqi Li ◽  
...  

AbstractLight therapy has been accepted as a promising therapeutic choice for depression. Positron emission tomography (PET) combined with specific radiotracers has great benefits for revealing pathogenesis and developing therapeutics. This study aimed to investigate the influences of light therapy on microglial activation and glucagon-like peptide-1 receptor (GLP-1R) expression in the brain of depressive rats using [18F]DPA-714 and [18F]exendin-4 PET. The results showed that chronic unpredictable mild stress (CUMS)-induced depressive rats had poorer performance in behavioral tests compared to normal rats (p < 0.05) and the depressive-like behavior could be ameliorated by light therapy. Besides, depressive rats had significantly higher [18F]DPA-714 uptake and lower [18F]FDG uptake compare to normal rats in 11 and 9 regions of interest (ROIs) of the brain, respectively (p < 0.05). After 5 weeks of light therapy, higher [18F]FDG and [18F]exendin-4 uptake was observed in most ROIs of light therapy-treated depressive rats compared to untreated depressive rats (p < 0.05) and no significant differences existed in [18F]DPA-714 uptake between the two groups. This study demonstrated that light therapy can ameliorate depressive-like behavior, improve glucose metabolism, and halt the decline of brain GLP-1R expression of depressive rats, but have no effects on microglial activation caused by CUMS. Besides, this study validated that [18F]DPA-714 and [18F]exendin-4 PET have the potential for noninvasive evaluation of microglial activation and GLP-1R expression in the brain of depression.


2017 ◽  
Vol 37 (10) ◽  
pp. 3401-3408 ◽  
Author(s):  
Shi Shu ◽  
Li Zhang ◽  
Yi Cheng Zhu ◽  
Fang Li ◽  
Li Ying Cui ◽  
...  

Angiogenesis is a critical compensation route, which has been demonstrated in the brain following ischemic stroke; however, few studies have investigated angiogenesis in chronic intracranial atherosclerosis disease (ICAD). We used 68Ga-NOTA-PRGD2 positron emission tomography/computed tomography based imaging to detect angiogenesis in chronic ICAD and to explore the factors that may have affected it. A total of 21 participants with unilateral severe chronic ICAD were included in the study. Of the 21 participants, 19 were men; the mean (SD) age was 52 (15) years. In 18 participants, we observed elevated 68Ga-NOTA-PRGD2 uptake in the peri-infarct, subcortical, and periventricular regions of the lesioned side, with a higher 68Ga-NOTA-PRGD2 SUVmax compared to that in the contralateral hemisphere (0.15 vs. 0.06, p=0.001). The 18F-FDG PET SUVmax was significantly lower on the lesioned side (11.28 vs. 13.92, p=0.001). Subgroup analyses revealed that the recent group (<6 months) had a higher lesion-to-contralateral region ratio SUVmax than the remote group (>6 months) (6.73 vs. 2.36, p<0.05). Our results provide molecular imaging evidence of angiogenesis in patients with severe chronic ICAD. Furthermore, the extent of angiogenesis in chronic ICAD may be affected by the post-qualified event time interval, and not by infarction itself or the severity of the arterial lesion.


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