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L. Trevor Young

Researcher at University of Toronto

Publications -  144
Citations -  16200

L. Trevor Young is an academic researcher from University of Toronto. The author has contributed to research in topics: Bipolar disorder & Lithium (medication). The author has an hindex of 62, co-authored 143 publications receiving 15122 citations. Previous affiliations of L. Trevor Young include University of British Columbia & Mental Health Research Institute.

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Number of manic episodes is associated with elevated DNA oxidation in bipolar I disorder

TL;DR: DNA 8-OHdG levels were higher in BD patients compared to healthy controls and found to be positively influenced by number of previous manic episodes, suggesting that oxidative damage to 8- OHdG might be a potential marker of disease progression, although further prospective cross-sectional studies to confirm neuroprogression in BD are warranted.
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Bipolar II Disorder: Symptoms, Course, and Response to Treatment

TL;DR: Preliminary studies suggest that the newer anticonvulsants may be of benefit for patients with bipolar II disorder, while other data suggest that there may be a greater role for antidepressant medications.
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Toward clinically applicable biomarkers in bipolar disorder: focus on BDNF, inflammatory markers, and endothelial function.

TL;DR: The adolescent population is a key focus as identifying biomarkers before the onset of comorbid medical conditions and which may help direct early intervention seem especially promising, suggesting a systematic approach to biomarker development in mood disorders is clearly warranted.
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Glutathione S-transferase is a novel target for mood stabilizing drugs in primary cultured neurons

TL;DR: Regulation of GST M1, and possibly GST’A4, may mediate the anti‐oxidative effects of valproate treatment, and regulation of GST may be involved in the mood stabilizing effect of valProate and lithium.
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The neurobiology of bipolar disorder: identifying targets for specific agents and synergies for combination treatment.

TL;DR: The data suggested that BD might be associated with neuronal and glial cellular impairment in specific brain areas, including the prefrontal cortex, and how these molecular pathways interact and their connection to the complex clinical manifestations observed in BD is attempted.