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Aye Mu Myint

Researcher at Ludwig Maximilian University of Munich

Publications -  40
Citations -  3996

Aye Mu Myint is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Kynurenine pathway & Kynurenine. The author has an hindex of 23, co-authored 39 publications receiving 3498 citations. Previous affiliations of Aye Mu Myint include University of Antwerp & Maastricht University Medical Centre.

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Kynurenine pathway in major depression: evidence of impaired neuroprotection.

TL;DR: In this article, the neurodegeneration hypothesis was proposed for major depression as a consequence of imbalance between neuroprotective and neuro-degenerative metabolites in the kynurenine pathway.
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The role of pro-inflammatory cytokines in neuroinflammation, neurogenesis and the neuroendocrine system in major depression.

TL;DR: Although current evidence strongly suggests that cytokines and GRs have important roles in depression, they are essential components of a whole system of inflammatory and endocrine interactions, rather than playing independent parts.
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Cytokine–serotonin interaction through IDO: a neurodegeneration hypothesis of depression

TL;DR: The cytokine-serotonin interaction that leads to the challenge between quinolinate and kynurenate in the brain explains the neurodegeneration hypothesis of depression.
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Imbalance between pro-inflammatory and anti-inflammatory cytokines in bipolar disorder.

TL;DR: It is suggested that the increased activity of pro- inflammatory cytokines and an imbalance between pro-inflammatory and anti-inflammatory cytokines may play a role in the pathophysiology of bipolar disorder.
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Interleukin-1β: a new regulator of the kynurenine pathway affecting human hippocampal neurogenesis.

TL;DR: It is shown for the first time how IL-1β, a pro-inflammatory cytokine shown to be increased in depressed patients, decreases neurogenesis in human hippocampal progenitor cells, and inhibition of the kynurenine pathway may provide a new therapy to revert inflammatory-induced reduction in Neurogenesis.