In vivo glutathione levels in young persons with bipolar disorder: A magnetic resonance spectroscopy study

Lagopoulos, Jim; Hermens, Daniel F.; Tobias-Webb, Juliette; Duffy, Shantel L.; Naismith, Sharon L.; White, Django; Scott, Elizabeth; Hickie, Ian B.

doi:10.1016/j.jpsychires.2012.12.006

Cited by 49 publications

(35 citation statements)

References 35 publications

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“…[38,39] These findings are inconsistent with studies from other groups finding increased oxidative stress in older samples with illness duration of 10 years on average [20] indicating that oxidative stress may be an outcome of long illness duration and repeated affective episodes rather than being a core feature of the pathophysiology of BD at onset.…”

Section: Discussionmentioning

confidence: 68%

“…Six additional studies examined the role of oxidative stress, inflammatory cytokines and BDNF in the pathophysiology of early-onset BD during adult age. [10,36,[38][39][40][41] Concordant findings showed that inflammatory m a r ke r s a r e i n c r e a s e d s i n c e t h e e a r l i e r stages of BD with: (1) increased TNF-α gene expression in adolescent BD showing aggressive behaviors; [35] (2) increased TNF-α levels in young adults with bipolar depression; [36] (3) increased TNF-α levels since the earlier stages of BD; [10] and (4) positive correlations between TNF-α levels and length of bipolar illness. [10] Also, increased levels of hsCRP have been detected in juvenile BD patients during manic and mixed episodes.…”

Section: Discussionmentioning

confidence: 99%

“…[10] Oxidative stress Two studies about the measurement of glutathione (GSH) concentrations in young adult patients with BD compared to healthy subjects suggested that there was no difference in GSH level in the ACC between patients and controls. [38,39] They reported that GSH levels were not correlated with depressive and manic episode severity [38] and were not significantly different between unmedicated and medicated subjects. [39] Also, they found that GSH levels were decreased in bipolar subjects with high levels of alcohol intake.…”

Section: Main Findingsmentioning

confidence: 99%

“…Decreased GSH in the ACC of high risk drinkers BD subjects No differences in GSH concentration between BD subjects and HCs Lagopoulos et al [38] Crosssectional n = 104 (13 BD-I; 25 BD-II; 15 BP-spectrum; 51 HC) inclusion and exclusion criteria and were included in this review. Table 1 provides the characteristics of each study, number of included subjects, diagnosis at baseline, age range of the subject sample, considered inflammatory/ oxidative stress markers or neurotrophins, and main findings of the considered study.…”

Section: Gshmentioning

confidence: 99%

See 3 more Smart Citations

The role of neuroinflammation in juvenile bipolar disorder

Serra¹,

Chiara²,

Marangoni³

et al. 2015

Neuroimmunol Neuroinflammation

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Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Section: Main Findingsmentioning

confidence: 99%

Section: Gshmentioning

confidence: 99%

See 2 more Smart Citations

The role of neuroinflammation in juvenile bipolar disorder

Serra¹,

Chiara²,

Marangoni³

et al. 2015

Neuroimmunol Neuroinflammation

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“…Recent evidences support that the cellular effects of oxidative stress worsen with time and number of manic episodes. Despite unchanged levels of the main cerebral antioxidant glutathione were found in the anterior cingulate cortex of BD patients in comparison with healthy controls [99], Rosa and collaborators, using blood samples from patients with different ages of disease onset, showed that glutathione levels are lower in BD patients and observed a negative correlation with the age at onset [100]. In addition, higher protein carbonyl and lipid hydroperoxide content were determined in adults compared to adolescents with BD [101] and the increased levels of an early component of the peroxidation chain in euthymic older patients with BD support the hypothesis of a persistent effect of ROS in patients with BD into late life [102].…”

Section: Oxidative Stressmentioning

confidence: 80%

The ups and downs of cellular stress: the “MAM hypothesis” for Bipolar disorder pathophysiology

Pereira¹,

Resende²,

Morais³

et al. 2017

IJCNMH

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Mental health problems constitute the largest single source of world economic burden, with an estimated global cost greater than cardiovascular disease, cancer or diabetes individually. In the European Union mental disorders affect millions of people and these numbers are expected to rise as result of Europe's ageing population. Given the biological causes of many of these disorders, most studies focus on their molecular basis. Bipolar disorder (BD) is characterized by mood swings between depression and mania resulting in cognitive and functional impairments that require lifetime treatment. Recurrent mood episodes, residual symptoms, functional impairment, psychosocial disability with high rates of divorce, unemployment, drug abuse and suicide attempting, and significant medical comorbidities such as metabolic and cardiovascular diseases cannot be efficiently controlled even with proper use of current treatments. Moreover, delayed diagnosis/misdiagnosis is frequent because reliable biomarkers are absent. Therefore, a better understanding of BD pathophysiology is a prerequisite for the design of new drugs and their implementation in clinical practice as well as to develop biomarkers for a more accurate and earlier diagnosis and/or evaluation of therapeutic response. This review summarises the association between decreased cellular resilience towards stress and BD. Since the key stress-response mediator Mitochondria-Associated Membranes (MAMs) modulate several BD relevant processes such as mitochondrial dysfunction and oxidative stress, Ca 2+ deregulation and cytoskeleton abnormalities, endoplasmic reticulum stress responses, loss of proteostasis and inflammasome activation, we propose the "MAM hypothesis" for BD pathophysiology. Targeting MAM-associated signaling pathways can be a promising investigation avenue to identify novel therapeutic strategies.Keywords: Bipolar disorder, Endoplasmic reticulum, Mitochondria, Mitochondria-associated membranes, Cellular resilience, Cellular stress, Plasticity. Bipolar DisorderBD is a chronic psychiatric illness with a remitting course, affecting 2.4% of the general population [1], characterized by mood swings between manic and depressive states that result in cognitive and functional impairments, high health care costs and premature mortality [2,3]. BD is the sixth leading cause of disability worldwide responsible for loss of more disability-adjusted life-years than all forms of cancer and major neurological conditions [4]. BD is associated with greatly impaired quality of life and increased physical health burden [5]. Moreover, BD patients tend to have high rates of divorce, unemployment, drug abuse and crime as consequence of impaired social cognition, and its impact on patients can be devastating, with approximately 23% of patients with BD reported having suicide attempts [6]. Moreover, individuals with BD diagnosis have a high risk of medical comorbidities such as metabolic (diabetes, obesity and metabolic syndrome) and cardiovascular disorders [7].Current knowl...

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