Molecular Biology of Bipolar Disorder

Andreazza, Ana C.; Wang, Jun Feng; Young, Trevor

doi:10.1002/9780470661277.ch17

Cited by 3 publications

(4 citation statements)

References 172 publications

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“…Our results should be interpreted in the context of inherent limitations of our samples and methods. First, some of these reported changes could be related to lower brain pH, which is commonly associated with ante-mortem agonal states, post-mortem delay, and storage of tissue (Andreazza et al 2010). In our samples, pH, PMI, age, and gender did not show a relationship with GST Pi or GST Mu levels.…”

Section: Discussionmentioning

confidence: 45%

“…GST Mu levels were not altered in BD patients in contrast to those with other diagnoses. This suggests a difference in this patient group in the capacity to detoxify through the GST system, as oxidative stress is increased in BD (Andreazza et al 2010). It is somewhat surprising that GST Mu levels were not altered in this group, suggesting some ability of the GST system to detoxify oxidized products in this illness.…”

Section: Discussionmentioning

confidence: 80%

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Prefrontal cortex glutathione S-transferase levels in patients with bipolar disorder, major depression and schizophrenia

Gawryluk

Wang

Andreazza

et al. 2011

Int. J. Neuropsychopharm.

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Antioxidant defence systems have received increasing attention in the pathophysiology of psychiatric disorders, including: bipolar disorder (BD), major depressive disorder (MDD), and schizophrenia (SCZ). Recently, we reported decreased glutathione (GSH) levels in post-mortem prefrontal cortex from patients with BD, MDD, and SCZ. To explore this further, we evaluated the levels of two glutathione S-transferase (GST) isoforms via immunoblotting: GST Pi and GST Mu. GST Pi levels were not affected in any of the patients groups vs. controls. GST Mu levels were significantly decreased in patients with MDD and SCZ but not BD. Compared to controls, GST Mu levels were not different in BD patients who had been treated with mood stabilizers at the time of death but were significantly lower in those not taking mood stabilizers at the time of death. These data suggest that GST Mu may be a target for mood stabilizers.

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Section: Discussionmentioning

confidence: 45%

Section: Discussionmentioning

confidence: 80%

Prefrontal cortex glutathione S-transferase levels in patients with bipolar disorder, major depression and schizophrenia

Gawryluk

Wang

Andreazza

et al. 2011

Int. J. Neuropsychopharm.

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“…Recent data showed increased oxidation and nitration of mitochondrial proteins in post-mortem prefrontal cortex from BD subjects (Andreazza et al 2010). In addition, a study using cultured rat cortical cells has also shown that valproate may prevent protein oxidation (Wang et al 2003).…”

Section: Oxidative Stress In Bipolar Disordermentioning

confidence: 98%

Morphometric post-mortem studies in bipolar disorder: possible association with oxidative stress and apoptosis

Gigante

Young

Yatham

et al. 2010

Int. J. Neuropsychopharm.

123

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Despite extensive research in the last decades, the pathophysiology of bipolar disorder (BD) remains unclear. Access to post-mortem brain tissue of subjects who had BD offers an opportunity to investigate neurobiology and this approach has led to some progress, particularly, due to the availability of more sophisticated molecular and cellular biological methodologies and well characterized brain collections over the past decade. Here we review the findings of morphometric post-mortem studies in BD and interpret them in the context of a potential physiopathological mechanism involving oxidative stress and apoptosis. A review of the literature was conducted to identify post-mortem studies that investigated cellular changes such as number, density and size of neurons and glia, in brains of subjects with BD. We found decreased density of neurons and glia and decreased size of neurons in frontal and subcortical areas of the brain. Based on recent studies that found evidence of increased apoptosis and oxidative stress in BD, we hypothesize that the cell abnormalities described are due to an increase in the apoptotic process that can be triggered, through its intrinsic pathway, by the existence of an exacerbated production of reactive oxygen species and oxidative damage in the disease.

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“…Lithium has been the gold standard in the treatment of bipolar disorder for more than 60 years, with solid evidence for mood‐stabilizing effects . There is strong evidence from in vitro and animal studies that lithium downregulates the enzyme glycogen synthase kinase‐3β (GSK3β) . GSK3β is involved in glycogen synthesis and in the regulation of critical intracellular signaling pathways, including cell cycle control, cell differentiation, gene expression, inflammation, and apoptosis, and several of these intracellular pathways seem to be disrupted in bipolar disorder, resulting in reduced neuroplasticity and neural atrophy …”

mentioning

confidence: 99%

Glycogen synthase kinase‐3β in patients with bipolar I disorder: results from a prospective study

et al. 2016

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Molecular Biology of Bipolar Disorder

Cited by 3 publications

References 172 publications

Prefrontal cortex glutathione S-transferase levels in patients with bipolar disorder, major depression and schizophrenia

Prefrontal cortex glutathione S-transferase levels in patients with bipolar disorder, major depression and schizophrenia

Morphometric post-mortem studies in bipolar disorder: possible association with oxidative stress and apoptosis

Glycogen synthase kinase‐3β in patients with bipolar I disorder: results from a prospective study

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