PET measurements of brain glucose metabolism and blood flow in major depressive disorder: a critical review

Videbech, Poul

doi:10.1034/j.1600-0447.2000.101001011.x

Cited by 371 publications

(221 citation statements)

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“…Hypofrontality, increased left and decreased right lentiform nucleus metabolic rate, and decreased temporal lobe metabolic rate have been reported in subjects with SZ compared to controls (for review, see (54)). In major depressive disorder, reduced metabolic rate has been observed in the prefrontal cortex, anterior cingulate cortex, and caudate nucleus in depressed patients (for review, see (55)). Similarly, depressed subjects with BPD display reduced whole-brain metabolism compared to manic subjects with BPD.…”

Section: Altered Metabolic Activitymentioning

confidence: 99%

Mitochondrial involvement in psychiatric disorders

et al. 2008

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Recent findings of mitochondrial abnormalities in brains from subjects with neurological disorders have led to a renewed search for mitochondrial abnormalities in psychiatric disorders. A growing body of evidence suggests that there is mitochondrial dysfunction in schizophrenia, bipolar disorder, and major depressive disorder, including evidence from electron microscopy, imaging, gene expression, genotyping, and sequencing studies. Specific evidence of dysfunction such as increased common deletion and decreased gene expression in mitochondria in psychiatric illnesses suggests that direct examination of mitochondrial DNA from postmortem brain cells may provide further details of mitochondrial alterations in psychiatric disorders.

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Section: Altered Metabolic Activitymentioning

confidence: 99%

Mitochondrial involvement in psychiatric disorders

et al. 2008

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“…[94][95][96][97][98] The regions most commonly affected in MDD were the prefrontal cortex, anterior cingulate gyrus, and temporal lobe, with contrasting results in subregions of these areas: Is brain energy metabolism involved in effective disorders? A Moretti et al 1. decreases in the dorsomedial, lateral and dorsolateral prefrontal cortex, dorsal anterior cingulate cortex, and hippocampus; 2. increases in the left ventrolateral prefrontal, subgenual prefrontal cortex (after correcting for volume reduction 99 ), amygdala, and thalamus.…”

Section: Neuroimaging In Affective Disorders and Therapymentioning

confidence: 99%

Affective disorders, antidepressant drugs and brain metabolism

2003

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There is increasing evidence that affective disorders are associated with dysfunction of neurotransmitter postsynaptic transduction pathways and that chronic treatment with clinically active drugs results in adaptive modification of these pathways. Despite the close dependence of signal transduction on adenosine triphosphate (ATP) availability, the changes in energy metabolism in affective disorders are largely unknown. This question has been indirectly dealt with through functional imaging studies (PET, SPECT, MRS). Despite some inconsistencies, PET and SPECT studies suggest low activity in cortical (especially frontal) regions in depressed patients, both unipolar and bipolar, and normal or increased activity in the manic pole. Preliminary MRS studies indicate some alterations in brain metabolism, with reduced creatine phosphate and ATP levels in the brain of patients with affective disorders. However, the involvement of the energy metabolism in affective disorders is still debated. We propose direct neurochemical investigations on mitochondrial functional parameters of energy transduction, such as the activities of (a) the enzymatic systems of oxidative metabolic cycle (Kreb's cycle); (b) the electron transfer chain; (c) oxidative phosphorylation, and (d) the enzyme activities of ATP-requiring ATPases. These processes should be studied in affective disorders and in animals treated with antidepressant drugs or lithium.

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“…While the performance of externally-cued, cognitive tasks is known to be impaired in patients with depression (Harvey et al 2005), the tonic nature of these core depressive symptoms has also prompted a wealth of resting-state imaging studies (Mayberg 2003;Videbech 2000). The bulk of these studies have been done using positron emission tomography (PET) to measure glucose metabolism and typically show that depressed subjects have reduced lateral prefrontal metabolism and increased medial prefrontal and subgenual cingulate metabolism (Mayberg 1997;Mayberg 2003).…”

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confidence: 99%

Resting-State Functional Connectivity in Major Depression: Abnormally Increased Contributions from Subgenual Cingulate Cortex and Thalamus

Greicius

Flores

Menon

et al. 2007

Biological Psychiatry

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Background: Positron emission tomography (PET) studies of major depression have revealed resting-state abnormalities in the prefrontal and cingulate cortices. Recently, fMRI has been adapted to examine connectivity within a specific resting-state neural network-the default-mode network -that includes the medial prefrontal and anterior cingulate cortices. The goal of this study was to examine resting-state, default-mode network functional connectivity in subjects with major depression and in healthy comparison subjects.

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PET measurements of brain glucose metabolism and blood flow in major depressive disorder: a critical review

Abstract: This evidence is consistent with the hypothesis that depressive symptoms are caused by dysfunction of regions of the limbic system and the frontal lobes in close connection with the basal ganglia.

Cited by 371 publications

References 0 publications

Mitochondrial involvement in psychiatric disorders

Mitochondrial involvement in psychiatric disorders

Affective disorders, antidepressant drugs and brain metabolism

Resting-State Functional Connectivity in Major Depression: Abnormally Increased Contributions from Subgenual Cingulate Cortex and Thalamus

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