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A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression.
TLDR
Robust and rapid antidepressant effects resulted from a single intravenous dose of an N-methyl-D-aspartate antagonist; onset occurred within 2 hours postinfusion and continued to remain significant for 1 week.
Targeting the glutamatergic system to develop novel, improved therapeutics for mood disorders
TLDR
There is growing evidence that the glutamatergic system is central to the neurobiology and treatment of mood disorders and exciting new prospects for the development of improved therapeutics for these devastating disorders are discussed.
A randomized add-on trial of an N-methyl-D-aspartate antagonist in treatment-resistant bipolar depression.
TLDR
In patients with treatment-resistant bipolar depression, robust and rapid antidepressant effects resulted from a single intravenous dose of an N-methyl-D-aspartate-receptor antagonist.
New insights into BDNF function in depression and anxiety
TLDR
BDNF may be a target of antidepressants, but not the sole mediator of depression or anxiety, and as the precursor proBDNF and the mature protein mBDNF can elicit opposite effects on cellular functions, the impact of proBD NF and its cleavage on mood should be considered.
The cellular neurobiology of depression
TLDR
This work has shown that antagonists designed to directly target molecules in signaling pathways that regulate neuroplasticity and cell survival in major depressive disorders may hold promise as new therapeutics for depression.
Discovering Endophenotypes for Major Depression
TLDR
The case is made for the development of a new classification system in order to reduce the heterogeneity of depression representing a major impediment to elucidating the genetic and neurobiological basis of this common, severe, and often life-threatening illness.
Preclinical models: status of basic research in depression
The Mood‐Stabilizing Agents Lithium and Valproate RobustlIncrease the Levels of the Neuroprotective Protein bcl‐2 in the CNS
TLDR
These novel findings represent the first report of medication‐induced increases in CNS bcl‐2 levels and may have implications not only for mood disorders, but also for long‐term treatment of various neurodegenerative disorders.
The Role of the Extracellular Signal-Regulated Kinase Signaling Pathway in Mood Modulation
TLDR
Lithium- and valproate-induced behavioral changes are qualitatively similar to the changes induced by amphetamine, a compound that induces relapse in remitted manic patients and mood elevation in normal subjects, suggesting that the ERK pathway may mediate the antimanic effects of mood stabilizers.
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