Targeting the glutamatergic system to develop novel, improved therapeutics for mood disorders

By G. Sanacora, C. Zarate, John H. Krystal, Husseini K. Manji. Nature reviews. Drug discovery, 2008

900 citations recorded by the source corpus.

Subfields: Biological Psychiatry, Cellular and Molecular Neuroscience, Pharmacology

View Paper: https://www.semanticscholar.org/paper/767c36745bfc0bc0a351904f186d2b1509bd5c44

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In Biological Psychiatry

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Citations in the corpus

A Randomized Add-on Trial of an N-methyl-d-aspartate Antagonist in Treatment-Resistant Bipolar Depression (2010, neutral): “Lithium 7 (39) 16 (89) Antidepressants Duloxetine 7 (39) 13 (72) SSRI 6 (33) 18 (100) Bupropion 5 (28) 16 (89) Venlafaxine 2 (11) 11 (61) Trazodone 2 (11) 7 (39) MAOI 1 (6) 7 (39) TCA 0 7 (39) Mirtazapine 0 6 (33) Nefazodone 0 3 (17) Antipsychotics Quetiapine 9 (50) 16 (89) Aripiprazole 2 (11) 10 (5”
Treatment-resistant depression: therapeutic trends, challenges, and future directions (2012, positive): “A number of drugs, including riluzole, that act on glutamate receptors and have antidepressant activity have also been developed and are approved for managing major depression.(81,130) Studies have explored the role of ketamine, an NMDA antagonist, in treating treatment-resistant depression and acut”
Towards a glutamate hypothesis of depression (2011, background): “…noted that while all antidepressant agents available on the market have a monoamine-based mechanism or at least a monoamine-based component in their mechanism (Racagni and Popoli, 2008; Sanacora et al., 2008), there are no approved antidepressant agents directly targeting the glutamatergic system.”
The neurobiology of psychedelic drugs: implications for the treatment of mood disorders (2010, background): “Ketamine therapy could be extended to other disorders in which NMDA receptors are implicated in the pathophysiology — for example, bipolar disorde”
The stressed synapse: the impact of stress and glucocorticoids on glutamate transmission (2011, background): “These findings suggest a new line of drug development that should be aimed at minimizing the effects of chronic stress exposure on the function of the glutamatergic neurotransmitter syste”
The Link between Depression and Chronic Pain: Neural Mechanisms in the Brain (2017, background): “Glutamate functions as one of the main excitatory neurotransmitters in the CNS and exists in synapses throughout the brain [48].”
Replication of Ketamine’s Antidepressant Efficacy in Bipolar Depression: A Randomized Controlled Add-on Trial (2012, background): “Over the past decade, findings from preclinical, postmortem, nd clinical studies have consistently implicated the glutamatergic ystem as a prime target system for developing the next generation f antidepressants, particularly by targeting the N-methyl-D-asparate (NMDA) receptor complex (6).”
Altered connectivity in depression: GABA and glutamate neurotransmitter deficits and reversal by novel treatments (2019, background): “Based in part on evidence of excitatory neuronal deficits, agents that act as glutamate AMPAR positive allosteric modulators (PAMs) have been developed and shown to have efficacy in rodent models (Sanacora et al., 2008).”
Frontocingulate Dysfunction in Depression: Towards Biomarkers of Treatment Response (2010, background): “In light of an emerging role of glutamate in the pathophysiology of MDD and the mechanism of action of antidepressants (Hashimoto, 2009; Sanacora et al, 2008), future studies are needed to understand the significance of these findings and explore the relevance of these neurochemical abnormalities…”