Brain Monoamine Oxidase A Binding in Major Depressive Disorder

Meyer, Jeffrey H.; Wilson, Alan A.; Sagrati, Sandra; Miler, Laura; Rusjan, Pablo; Bloomfield, Peter; Clark, Michael E.; Sacher, Julia; Voineskos, Aristotle N.; Houle, Sylvain

doi:10.1001/archgenpsychiatry.2009.156

Cited by 168 publications

(54 citation statements)

References 66 publications

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“…Altogether, our results demonstrate that insufficient dietary iron supply can establish molecular features that resemble several neurological disorders, such as abnormal ferritin accumulation in striatum observed in parkinsonian syndromes and Huntington disease (Vidal et al, 2004; Simmons et al, 2007), increased MAO-A activity in prefrontal cortex which is associated with depression (Meyer et al, 2009) and increased degree of lipid peroxidation in hippocampus that is related with most of conformational diseases (Sultana et al, 2013). By showing these molecular alterations, this study emphasizes the importance of adequate iron supplementation for brain health and prevention of neurological diseases.…”

Section: Discussionmentioning

confidence: 53%

“…Previous studies have demonstrated that iron chelators can reduce the MAO activity, suggesting that iron bioavailability can affect the MAO activity (Zheng et al, 2005; Gal et al, 2006). The underlying mechanism of induction of MAO-A activity in IR group is still unclear, but these results can help to explain the symptoms of depression reported in iron-deficient population (Corwin et al, 2003), since increased MAO-A activity has been linked to mood disorders (Meyer et al, 2009; Sacher et al, 2015; Kolla et al, 2016). …”

Section: Discussionmentioning

confidence: 99%

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Iron-Restricted Diet Affects Brain Ferritin Levels, Dopamine Metabolism and Cellular Prion Protein in a Region-Specific Manner

Pino

Luz

Antunes

et al. 2017

Front. Mol. Neurosci.

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Iron is an essential micronutrient for several physiological functions, including the regulation of dopaminergic neurotransmission. On the other hand, both iron, and dopamine can affect the folding and aggregation of proteins related with neurodegenerative diseases, such as cellular prion protein (PrPC) and α-synuclein, suggesting that deregulation of iron homeostasis and the consequential disturbance of dopamine metabolism can be a risk factor for conformational diseases. These proteins, in turn, are known to participate in the regulation of iron and dopamine metabolism. In this study, we evaluated the effects of dietary iron restriction on brain ferritin levels, dopamine metabolism, and the expression levels of PrPC and α-synuclein. To achieve this goal, C57BL/6 mice were fed with iron restricted diet (IR) or with normal diet (CTL) for 1 month. IR reduced iron and ferritin levels in liver. Ferritin reduction was also observed in the hippocampus. However, in the striatum of IR group, ferritin level was increased, suggesting that under iron-deficient condition, each brain area might acquire distinct capacity to store iron. Increased lipid peroxidation was observed only in hippocampus of IR group, where ferritin level was reduced. IR also generated discrete results regarding dopamine metabolism of distinct brain regions: in striatum, the level of dopamine metabolites (DOPAC and HVA) was reduced; in prefrontal cortex, only HVA was increased along with the enhanced MAO-A activity; in hippocampus, no alterations were observed. PrPC levels were increased only in the striatum of IR group, where ferritin level was also increased. PrPC is known to play roles in iron uptake. Thus, the increase of PrPC in striatum of IR group might be related to the increased ferritin level. α-synuclein was not altered in any regions. Abnormal accumulation of ferritin, increased MAO-A activity or lipid peroxidation are molecular features observed in several neurological disorders. Our findings show that nutritional iron deficiency produces these molecular alterations in a region-specific manner and provide new insight into the variety of molecular pathways that can lead to distinct neurological symptoms upon iron deficiency. Thus, adequate iron supplementation is essential for brain health and prevention of neurological diseases.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Iron-Restricted Diet Affects Brain Ferritin Levels, Dopamine Metabolism and Cellular Prion Protein in a Region-Specific Manner

Pino

Luz

Antunes

et al. 2017

Front. Mol. Neurosci.

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“…1,9,40 The ability to image and quantify human brain MAO A with PET has enabled the investigation of relationships between MAO A levels and behavioral and disease phenotypes in healthy volunteers and in patients. [41][42][43] For example, PET studies have revealed elevations in brain MAO A activity in major depressive disorder (MDD) 44 and mood disorders, 43 whereas low MAO A activity has been related to maladaptive behavioral traits, such as aggression. 45 Interestingly, PET imaging has also demonstrated a modulating effect of the environment on brain enzyme levels by showing that current cigarette smokers have reduced brain MAO A.…”

Section: Discussionmentioning

confidence: 99%

Evidence that the methylation state of the monoamine oxidase A (MAOA) gene predicts brain activity of MAO A enzyme in healthy men

Shumay

Logan

Volkow³

et al. 2012

Epigenetics

110

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“…Experiments that use a model of a depression like state that is induced by immunization of rats against complexes of exogenous or endogenous MAO inhibi tors with a protein carrier have shown that these animals have increased MAO activity [26]. Patients with depres sion have enhanced receptor binding of MAO A [27] and increased 5 HT turnover in the brain regions [28].…”

Section: Discussionmentioning

confidence: 99%

The levels of monoamines and their metabolites in the brain structures of rats with an experimental anxiodepressive state induced by administration of an inhibitor of dipeptidyl peptidase 4 in the early postnatal period

et al. 2012

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In a model of an experimental anxiodepressive state induced by postnatal administration of an inhibitor of dipeptidyl peptidase 4 (DPP 4), we studied peculiarities of the turnover of dopamine (DA), nora drenaline (NA), and serotonin (5 HT) in the brain structures of rats at ages of 1, 3, and 7 months. In males, the major changes in the functional activity of the DA system, which are related to a decrease in DA turnover according to the HVA/DA ratio, were observed in the striatum. In males at an age of 7 months, we found an increase in the NA level in the hypothalamus. In females, changes in the state of the DA system included a decrease in the level of DA and its metabolites in the nucleus accumbens (1 and 3 months), the level of DOPAC in the hypothalamus (3 months), and the level of DA in the striatum (7 months). At all ages, in the hippocampus of females, we found an increase in the functional activity of 5 HT, according to the 5 HIAA/5 HT and 5 HIAA level. In the frontal cortex of females at an age of 3 months we found a decrease in the 5 HIAA/5 HT ratio and an increase in the DOPAC/DA ratio, while at the age of 7 months, we observed an increase in 5 HT. These changes in the activity of the central monoaminergic systems may reflect specific features of the functioning of the pathological system of the anxiodepressive state in the CNS that determine the character of the formation and dynamics of emotional behavioral disturbances of male and female rats.

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Brain Monoamine Oxidase A Binding in Major Depressive Disorder

Cited by 168 publications

References 66 publications

Iron-Restricted Diet Affects Brain Ferritin Levels, Dopamine Metabolism and Cellular Prion Protein in a Region-Specific Manner

Iron-Restricted Diet Affects Brain Ferritin Levels, Dopamine Metabolism and Cellular Prion Protein in a Region-Specific Manner

Evidence that the methylation state of the monoamine oxidase A (MAOA) gene predicts brain activity of MAO A enzyme in healthy men

The levels of monoamines and their metabolites in the brain structures of rats with an experimental anxiodepressive state induced by administration of an inhibitor of dipeptidyl peptidase 4 in the early postnatal period

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