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Valina L. Dawson

Researcher at Johns Hopkins University School of Medicine

Publications -  477
Citations -  88024

Valina L. Dawson is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Neurodegeneration & Parkin. The author has an hindex of 136, co-authored 451 publications receiving 76986 citations. Previous affiliations of Valina L. Dawson include University of Baltimore & Hospital of the University of Pennsylvania.

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Inhibitors of poly(ADP-ribose) synthetase and use thereof to treat NMDA neurotoxicity

TL;DR: Inhibitors of poly(ADP-ribose) synthetase can be used to prevent neurotoxicity mediated through N-methyl-D-aspartate (NMDA) receptors as mentioned in this paper.
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Leucine-rich repeat kinase 2 (LRRK2) as a potential therapeutic target in Parkinson's disease.

TL;DR: The potential and feasibility of targeting LRRK2 as a therapeutic strategy for PD is discussed and it is becoming increasingly evident that aberrant kinase activity of the pathologic mutants of LRRk2 is associated with neurodegeneration, suggesting that the kinaseactivity of L RRK2 is a potential therapeutic target.
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Resistance to MPTP-neurotoxicity in α-synuclein knockout mice is complemented by human α-synuclein and associated with increased β-synuclein and Akt activation.

TL;DR: The in vivo interaction of mouse and human α-synuclein with the potent parkinsonian neurotoxin, MPTP is investigated to provide new mechanistic insights on the role α- synuclein in modulating neurodegenerative phenotypes by regulation of Akt-mediated cell survival signaling in vivo.
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MPTP and DSP-4 susceptibility of substantia nigra and locus coeruleus catecholaminergic neurons in mice is independent of parkin activity

TL;DR: It is reported that nigrostriatal dopaminergic neurons in parkin knockout mice do not show increased susceptibility to the parkinsonian neurotoxin, MPTP, in acute, subacute and chronic dose regimens of the neurotoxin.
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LRRK2 affects vesicle trafficking, neurotransmitter extracellular level and membrane receptor localization.

TL;DR: In neuronal cells, the presence of LRRK2G2019S pathological mutant determines increased extracellular dopamine levels either under basal conditions or upon nicotine stimulation, and ultrastructural analysis of PC12-derived cells expressing mutant LRRk2G 2019S shows an altered intracellular vesicle distribution.