Beyond the serotonin hypothesis: Mitochondria, inflammation and neurodegeneration in major depression and affective spectrum disorders

Gardner, Ann; Boles, Richard G.

doi:10.1016/j.pnpbp.2010.07.030

Cited by 287 publications

(189 citation statements)

References 218 publications

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“…Indeed, chronic administration of the tricyclic antidepressant imipramine in rats resulted in altered respiratory rates and increased ATP synthesis in brain mitochondria [39]. The significance of the correlation between mitochondrial functions and MDD has been emphasized recently [40,41], and our results are consistent with this correlation.…”

Section: Accepted M Manuscriptsupporting

confidence: 88%

Proteomic investigation of the prefrontal cortex in the rat clomipramine model of depression

Gellén

Völgyi

Győrffy

et al. 2017

Journal of Proteomics

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Section: Accepted M Manuscriptsupporting

confidence: 88%

Proteomic investigation of the prefrontal cortex in the rat clomipramine model of depression

Gellén

Völgyi

Győrffy

et al. 2017

Journal of Proteomics

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“…Moreover, neurotransmitter deficiency can be a primary cause of psychiatric disorders or entrain compensatory changes in receptor expression and synaptic structure that affect brain function. Neuronal energy depletion, osmotic dysregulation, and dysmyelination also likely contribute to the development of psychiatric disorders (Jou et al 2009;Gardner and Boles 2011). Additionally, major depression is characterized by significantly lower plasma concentrations of a number of key antioxidants, such as vitamin E, zinc, and coenzyme Q10.…”

Section: Discussionmentioning

confidence: 99%

Behavioral Responses in Rats Submitted to Chronic Administration of Branched-Chain Amino Acids

et al. 2013

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Maple syrup urine disease (MSUD) is an inborn metabolism error caused by a deficiency of branched-chain a-keto acid dehydrogenase complex activity. This blockage leads to an accumulation of the branched-chain amino acids (BCAA) leucine, isoleucine, and valine, as well as their corresponding a-keto and a-hydroxy acids. Previous reports suggest that MSUD patients are at high risk for chronic neuropsychiatric problems. Therefore, in this study, we assessed variables that suggest depressive-like symptoms (anhedonia as measured by sucrose intake, immobility during the forced swimming test and body and adrenal gland weight) in rats submitted to chronic administration of BCAA during development. Furthermore, we determined if these parameters were sensitive to imipramine and N-acetylcysteine/deferoxamine (NAC/DFX). Our results demonstrated that animals subjected to chronic administration of branched-chain amino acids showed a decrease in sucrose intake without significant changes in body weight. We also observed an increase in adrenal gland weight and immobility time during the forced swimming test. However, treatment with imipramine and NAC/DFX reversed these changes in the behavioral tasks. In conclusion, this study demonstrates a link between MSUD and depression in rats. Moreover, this investigation reveals that the antidepressant action of NAC/DFX and imipramine might be associated with their capability to maintain pro-/anti-oxidative homeostasis.

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“…Dietary antioxidants or caloric restriction, as well as chemical antioxidants, can lower mitochondrial ROS production (Vitetta and Anton, 2007). Nutrients such as CoQ10, vitamin B2 and l-carnitine also have a significant influence on mitochondrial metabolism (Gardner and Boles, 2011).…”

Section: Diet and Its Effect On Mitochondriamentioning

confidence: 99%

A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise

Lopresti

Hood

Drummond

2013

Journal of Affective Disorders

529

412

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Research on major depression has confirmed that it is caused by an array of biopsychosocial and lifestyle factors. Diet, exercise and sleep are three such influences that play a significant mediating role in the development, progression and treatment of this condition. This review summarises animal and human-based studies on the relationship between these three lifestyle factors and major depressive disorder, and their influence on dysregulated pathways associated with depression, namely neurotransmitter processes, immuno-inflammatory pathways, hypothalamic-pituitary-adrenal (HPA) axis disturbances, oxidative stress and antioxidant defence systems, neuroprogression, and mitochondrial disturbances. Increased attention in future clinical studies on the influence of diet, sleep and exercise on major depressive disorder and investigations of their effect on physiological processes will help to expand our understanding and treatment of major depressive disorder. Mental health interventions, taking into account the bidirectional relationship between these lifestyle factors and major depression are also likely to enhance the efficacy of interventions associated with this disorder.

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Beyond the serotonin hypothesis: Mitochondria, inflammation and neurodegeneration in major depression and affective spectrum disorders

Cited by 287 publications

References 218 publications

Proteomic investigation of the prefrontal cortex in the rat clomipramine model of depression

Proteomic investigation of the prefrontal cortex in the rat clomipramine model of depression

Behavioral Responses in Rats Submitted to Chronic Administration of Branched-Chain Amino Acids

A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise

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