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Thi Nguyet Anh Tran

Researcher at University of Texas Southwestern Medical Center

Publications -  12
Citations -  1203

Thi Nguyet Anh Tran is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Neurodegeneration & Parkin. The author has an hindex of 10, co-authored 12 publications receiving 1089 citations. Previous affiliations of Thi Nguyet Anh Tran include Charité.

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Neuroinflammation in Parkinson’s Disease

TL;DR: This review discusses the various hypotheses regarding the role of microglia and other immune cells in PD pathogenesis and progression, the inflammatory mechanisms implicated in disease progression from pre-clinical and clinical studies, the recent evidence that systemic inflammation can trigger microglian activation in PD-relevant central nervous system regions, and the latest update on meta-analysis of epidemiological studies on the risk-lowering effects of anti-inflammatory drug regimens.
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Parkin Deficiency Increases Vulnerability to Inflammation-Related Nigral Degeneration

TL;DR: The studies suggest that loss of Parkin function increases the vulnerability of nigral DA neurons to inflammation-related degeneration, which may enable identification of early biomarkers of degeneration and aid in preclinical screening efforts to identify compounds that can halt or delay the progressive degeneration of the nigrostriatal pathway.
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Mass-Spectrometric Identification of a Novel Angiotensin Peptide in Human Plasma

TL;DR: Ang A is a novel human strong vasoconstrictive angiotensin-derived peptide, most likely generated by enzymatic transformation through mononuclear leukocyte-derived aspartate decarboxylase, increased in end-stage renal failure patients.
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Neuroinflammation in Parkinson's disease: is there sufficient evidence for mechanism-based interventional therapy?

TL;DR: The neurotoxic role of microglia-derived inflammatory mediators which are suspected to hasten the death of nigral dopaminergic neurons are discussed, in particular the pro-inflammatory cytokine Tumor Necrosis Factor (TNF) and its downstream signaling pathways.
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The synthetic triterpenoid CDDO-methyl ester modulates microglial activities, inhibits TNF production, and provides dopaminergic neuroprotection.

TL;DR: The neuroimmune modulatory properties of CDDO-Me indicate that this potent antioxidant and anti-inflammatory compound may have therapeutic potential to modify the course of neurodegenerative diseases characterized by chronic neuroinflammation and amyloid deposition.