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Mattea L. Tan

Researcher at McMaster University

Publications -  7
Citations -  104

Mattea L. Tan is an academic researcher from McMaster University. The author has contributed to research in topics: Dopamine receptor D2 & Synapsin. The author has an hindex of 7, co-authored 7 publications receiving 95 citations.

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Preclinical pharmacokinetic and toxicological evaluation of MIF-1 peptidomimetic, PAOPA: examining the pharmacology of a selective dopamine D2 receptor allosteric modulator for the treatment of schizophrenia.

TL;DR: Results from this study prove the effectiveness of PAOPA in reaching the implicated regions of the brain for therapeutic action, particularly the striatum, and demonstrate a better safety profile ofPAOPA, and necessitates the progression of this newly developed therapeutic for the treatment of schizophrenia.
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Smith-Lemli-Opitz syndrome: Objective assessment of facial phenotype.

TL;DR: There were no significant differences in the craniofacial pattern profile between the sexes or clinical severity as measured by either plasma cholesterol level at the time of diagnosis or the physical severity score, suggesting that the degree of deviation from cranioFacial norms is a function of the overall physical severity.
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Curcumin prevents haloperidol-induced development of abnormal oro-facial movements: possible implications of Bcl-XL in its mechanism of action.

TL;DR: It is suggested that curcumin may be a promising treatment to prevent the development of AOFMs and further suggest some therapeutic value in the treatment of movement disorders.
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Role of AP-2α Transcription Factor in the Regulation of Synapsin II Gene Expression by Dopamine D1 and D2 Receptors

TL;DR: Results indicate that a cyclic adenosine-3′,5′-monophosphate/PKA-dependent mechanism involving the AP-2α transcription factor is likely responsible for the increase in neuronal synapsin II following dopamine D1 receptor stimulation or dopamine D2 receptor inhibition.
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Behavioral effects of non-viral mediated RNA interference of synapsin II in the medial prefrontal cortex of the rat.

TL;DR: The results reveal that rats with selective reductions in medial prefrontal cortical synapsin II demonstrate deficits in sensorimotor gating (prepulse inhibition), hyperlocomotion, and reduced social behavior, and suggest that increasing synpsin II levels in the medial prefrontal cortex may potentially serve as a novel therapeutic target for this devastating disorder.