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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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Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures.

TL;DR: It is established that NO mediates the neurotoxicity of glutamate and Hemoglobin, which complexes NO, prevents neurotoxic effects of both N-methyl-D-aspartate and sodium nitroprusside.
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Activation of memory circuits during cue-elicited cocaine craving

TL;DR: Correlations of metabolic increases in the dorsolateral prefrontal cortex, medial temporal lobe, and cerebellum with self-reports of craving suggest that a distributed neural network, which integrates emotional and cognitive aspects of memory, links environmental cues with cocaine craving.
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Genome-wide association meta-analysis in 269,867 individuals identifies new genetic and functional links to intelligence

Jeanne E. Savage, +135 more
- 25 Jun 2018 - 
TL;DR: A large-scale genetic association study of intelligence identifies 190 new loci and implicates 939 new genes related to neurogenesis, neuron differentiation and synaptic structure, a major step forward in understanding the neurobiology of cognitive function as well as genetically related neurological and psychiatric disorders.
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Gender-Linked Brain Injury in Experimental Stroke

TL;DR: It is concluded that endogenous estrogen improves stroke outcome during vascular occlusion by exerting both neuroprotective and flow-preserving effects.
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Structural Abnormalities in the Brains of Human Subjects Who Use Methamphetamine

TL;DR: MRI-based maps suggest that chronic methamphetamine abuse causes a selective pattern of cerebral deterioration that contributes to impaired memory performance, and brain substrates may help account for the symptoms of MA abuse, providing therapeutic targets for drug-induced brain injury.