Serotonin Modulation of Cerebral Glucose Metabolism in Depressed Older Adults

Smith, Gordon S.; Kramer, Efraim; Hermann, Carol; Ma, Yilong; Dhawan, Vijay; Chaly, Thomas; Eidelberg, David

doi:10.1016/j.biopsych.2009.02.012

Cited by 46 publications

(54 citation statements)

References 51 publications

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“…Furthermore, between-subject differences in medication existed, and it is known that selective reuptake inhibitors may induce metabolic decreases in the ACC, middle temporal cortex, precuneus, and parahippocampal region (37). However, since medication was kept low and stable during the imaging period, medication is unlikely to have been a confounder in the current results.…”

Section: Discussionmentioning

confidence: 61%

Differences in Metabolic Network Modulation Between Capsulotomy and Deep-Brain Stimulation for Refractory Obsessive-Compulsive Disorder

et al. 2014

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Around 7%-10% of patients with obsessive-compulsive disorder (OCD) are refractory to first-line treatment. Neurosurgical approaches are available such as capsulotomy or deep-brain stimulation (DBS). There is strong evidence for central involvement of the corticostriatopallidothalamocortical (CSPTC) circuit in OCD, but the exact mechanism through which these interventions lead to clinical improvement and potential differences in network modulation are not fully understood. Methods: In total, 13 capsulotomy patients (aged 29-59 y, 10 men and 3 women) and 16 DBS patients (aged 25-56 y, 6 men and 10 women) were prospectively included. 18 F-FDG PET was performed before and after capsulotomy and before and after DBS in both stimulation-on and stimulation-off conditions. Presurgical scans were compared with scans of healthy volunteers using SPM8 and global scaling, and metabolic changes after DBS were compared with changes after capsulotomy. Correlations with clinical improvements were investigated using the Yale-Brown ObsessiveCompulsive Scale (Y-BOCS) and the Hamilton Depression Rating Scale (HAM-D). Results: Both groups had similar pretreatment clinical morbidity as assessed by Y-BOCS and the Hamilton Depression Rating Scale. Preoperative superior frontal and supplementary motor cortex hypometabolism was common to both patient groups, and the subgenual anterior cingulate, occipital cortex (cuneus), and posterior cerebellum were relatively hypermetabolic. Postoperative metabolic decreases were common to both interventions in the anterior cingulate and the prefrontal and orbitofrontal cortices. Compared with DBS, capsulotomy resulted in more intense metabolic changes, with additional significant decreases in the mediodorsal thalamus, caudate nucleus, and cerebellum as well as increases in the precuneus and the fusiform and lingual gyrus. The stimulation-off condition of DBS patients showed no significant differences from the preoperative state. Improvement in Y-BOCS scores correlated with metabolic changes in the occipital cortex. Baseline metabolism in the subgenual anterior cingulate and superior temporal cortices were related to postoperative improvement of depressive symptoms. Conclusion: Capsulotomy and DBS lead to similar clinical improvement and similar metabolic network changes in the CSPTC circuit, with a prominent role for the subgenual anterior cingulate and other core structures of the CSPTC. However, metabolic changes are more pronounced and extended in capsulotomy than in DBS. Furthermore, cortical regions outside the CSPTC may also play an important role in OCD symptomatology.

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Section: Discussionmentioning

confidence: 61%

Differences in Metabolic Network Modulation Between Capsulotomy and Deep-Brain Stimulation for Refractory Obsessive-Compulsive Disorder

et al. 2014

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“…Aß(−) MCI subjects positive to depressive symptoms were mostly inconspicuous with regard to FDG metabolism. These results likely explain the inconsistent results in previous FDG-PET studies regarding late-life depression where Aß status was not hitherto considered: Either hypermetabolism [11-13, 24] or hypometabolism [14-17] have been reported in late-life depressed subjects both in cognitively preserved, and impaired and AD patients. Moreover, PVEC was not applied in these FDG-PET studies investigating this topic, such that atrophy, as may occur in depressed subjects [37, 38], may have resulted in spurious findings of hypometabolism.…”

Section: Discussionmentioning

confidence: 77%

“…Prior investigations regarding the link between depression and brain amyloidosis have mainly focused on subjects with remitted earlier depressive episodes [8-10], mostly finding elevated β-amyloid levels. Despite these roughly consistent amyloid PET findings, there is less concordance in [ 18 F]-fluorodeoxyglucose (FDG) PET studies in depressed subjects, which have shown regions of hypermetabolism [11-13] or hypometabolism [14-17]. …”

Section: Introductionmentioning

confidence: 99%

Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients

Brendel¹,

Pogarell

Xiong

et al. 2015

Eur J Nucl Med Mol Imaging

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Purpose Late-life depression (LLD) even in subsyndromal stages revealed strong associations with Alzheimer’s disease (AD). Furthermore brain amyloidosis depicts an early biomarker in subjects subsequently suffering from AD and is sensitively detectable by amyloid-PET. Therefore we aimed to compare amyloid-load and glucose metabolism in subsyndromally depressed mild cognitive impaired (MCI) subjects. Methods 371 MCI subjects from ADNI underwent [18F]-AV45-, [18F]-FDG-PET, and MRI. Subjects were judged β-amyloid positive (Aß(+); N=206) or negative (Aß(−); N=165) according to [18F]-AV45-PET. Depressive symptoms were assessed by the Neuropsychiatric Inventory Questionnaire (NPI-Q) depression-item. 65 Aß(+) and 41 Aß(−) subjects with depressive symptoms (DEP) were contrasted against their non-depressed (NON-DEP) counterparts. Conversion rates to AD were analysed (mean follow-up time: 21.5±9.1 months) with regard to coexisting depressive symptoms and brain amyloid-load. Results Aß(+) DEP subjects showed large clusters with higher amyloid-load in frontotemporal and insular cortices (p<0.001) and coincident hypermetabolism (p<0.001) in frontal cortices when contrasted against NON-DEP. Faster progression to AD was observed in subjects with either depressive symptoms (p<0.005) or Aß(+) status (p<0.001). Coincident depressive symptoms additionally shortened the conversion time in all Aß(+) subjects (p<0.005) and to a greater extent in a subgroup with high amyloid-load (p<0.001). Conclusions Our results clearly indicate that Aß(+) MCI subjects with depressive symptoms suffer from elevated amyloid-load combined with relative hypermetabolism of connected brain areas when contrasted against cognitively-matched non-depressed individuals. MCI subjects with high amyloid-load and coexistent depressive symptoms represent a high-risk group for faster conversion to AD.

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“…To evaluate significant differences, we used an approach with the peak threshold set at P ϭ .001 (uncorrected) for whole brain regions. 13,14 For hypothesis generation, we reported only clusters that survived an FDR correction at P Ͻ .05. Significant regions were localized by Talairach Daemon software (http://software.incf.org/software/talairach-daemon) after using a MNI-to-Talairach conversion tool.…”

Section: Discussionmentioning

confidence: 99%

Stability in Brain Glucose Metabolism Following Brown Adipose Tissue Inactivation in Chinese Adults

Miao

Zhao²,

Zhang³

et al. 2012

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:The thermogenesis of BAT is believed to be controlled through some pathways initiated in the brain, though the changes in brain activity among different states of BAT-positive subjects are still unclear. We hypothesized that some significant differences of regional cerebral metabolism between various groups were related to the BAT activities regardless of temperature changes.

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Serotonin Modulation of Cerebral Glucose Metabolism in Depressed Older Adults

Cited by 46 publications

References 51 publications

Differences in Metabolic Network Modulation Between Capsulotomy and Deep-Brain Stimulation for Refractory Obsessive-Compulsive Disorder

Differences in Metabolic Network Modulation Between Capsulotomy and Deep-Brain Stimulation for Refractory Obsessive-Compulsive Disorder

Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients

Stability in Brain Glucose Metabolism Following Brown Adipose Tissue Inactivation in Chinese Adults

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