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Edythe D. London

Researcher at University of California, Los Angeles

Publications -  492
Citations -  36481

Edythe D. London is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Nicotinic agonist & Methamphetamine. The author has an hindex of 93, co-authored 482 publications receiving 33741 citations. Previous affiliations of Edythe D. London include Icahn School of Medicine at Mount Sinai & Semel Institute for Neuroscience and Human Behavior.

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White-matter abnormalities in brain during early abstinence from methamphetamine abuse

TL;DR: The findings support the idea that methamphetamine abuse produces microstructural abnormalities in white matter underlying and interconnecting prefrontal cortices and hippocampal formation Already present during the first weeks of abstinence from methamphetamine are linked to psychiatric symptoms assessed during this period.
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Gender effects on mood and cigarette craving during early abstinence and resumption of smoking

TL;DR: It is indicated that overnight abstinence produces more negative mood symptoms and cigarette craving in female smokers than in males, and that resumption of smoking produces greater relief from these symptoms infemale smokers.
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Inhibitory control deficits in childhood and risk for substance use disorders: a review.

TL;DR: This review focuses on the relationship between impulsivity—a behavior that is common to the clinical picture of both substance use disorders (SUD) and childhood disruptive behavior disorders—and neurobiological risk for SUD, and concludes that underlying deficits in inhibitory control may be central to many of the behaviors associated with high risk with SUD.
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Dysregulation of D2-Mediated Dopamine Transmission in Monkeys after Chronic Escalating Methamphetamine Exposure

TL;DR: Evidence is provided that chronic, escalating-dose methamphetamine administration alters the dopamine system in a manner similar to that observed in methamphetamine-dependent humans and implicate alterations in positive-feedback sensitivity associated with D2-like receptor dysfunction as the mechanism by which inhibitory control deficits emerge in stimulant-dependent individuals.