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Amit Anand

Researcher at Cleveland Clinic

Publications -  182
Citations -  11052

Amit Anand is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Bipolar disorder & Mania. The author has an hindex of 43, co-authored 148 publications receiving 9622 citations. Previous affiliations of Amit Anand include United States Department of Veterans Affairs & Cleveland Clinic Lerner College of Medicine.

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Antidepressant effects of ketamine in depressed patients

TL;DR: A first placebo-controlled, double-blinded trial to assess the treatment effects of a single dose of an N-methyl-D-aspartate (NMDA) receptor antagonist in patients with depression suggests a potential role for NMDA receptor-modulating drugs in the treatment of depression.
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Activity and Connectivity of Brain Mood Regulating Circuit in Depression: A Functional Magnetic Resonance Study

TL;DR: The finding of increased activation of limbic regions and decreased LFBF correlations between ACC and limbic areas is consistent with the hypothesis that decreased cortical regulation of limbics activation in response to negative stimuli may be present in depression.
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Recent developments in biological activities of chalcones: a mini review.

TL;DR: This review article focuses on the recent developments (2010-2014) on various pharmacological and medicinal aspects of chalcones and their analogues.
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Glutamate and GABA systems as targets for novel antidepressant and mood-stabilizing treatments

TL;DR: The preponderance of available evidence suggests that glutamatergic and GABAergic modulation may be an important property of available antidepressant and mood-stabilizing agents.
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Attenuation of the Neuropsychiatric Effects of Ketamine With Lamotrigine: Support for Hyperglutamatergic Effects of N-methyl-D-aspartate Receptor Antagonists

TL;DR: The hypothesis that lamotrigine, a drug reported to inhibit glutamate release, will reduce the neuropsychiatric effects of ketamine in humans is tested and it is suggested that glutamate release-inhibiting drugs may reduce the hyperglutamatergic consequences of NMDA receptor dysfunction implicated in the pathophysiologic processes of neuro psychological illnesses such as schizophrenia.