Ionic Glutamate Modulators in Depression (Zinc, Magnesium)

2010 ◽  
pp. 21-38 ◽  
Author(s):  
Bernadeta Szewczyk ◽  
Ewa Poleszak ◽  
Andrzej Pilc ◽  
Gabriel Nowak
Keyword(s):  
Glutamate Modulators

scholarly journals Biomarkers of ketamine’s antidepressant effect: a clinical review of genetics, functional connectivity, and neurophysiology

2021 ◽  
Vol 5 ◽  
pp. 247054702110142
Author(s):  
Alexandra A. Alario ◽  
Mark J. Niciu
Keyword(s):  
Treatment Response ◽  
Antidepressant Treatment ◽  
A Priori ◽  
Antidepressant Effect ◽  
Aspartate Receptor ◽  
Neurophysiological Studies ◽  
All Cause Mortality ◽  
Antidepressant Efficacy ◽  
Glutamate Modulators ◽  
Response Biomarkers

Major depressive disorder (MDD) is one of the leading causes of morbidity and all-cause mortality (including suicide) worldwide, and, unfortunately, first-line monoaminergic antidepressants and evidence-based psychotherapies are not effective for all patients. Subanesthetic doses of the N-methyl-D-aspartate receptor antagonists and glutamate modulators ketamine and S-ketamine have rapid and robust antidepressant efficacy in such treatment-resistant depressed patients (TRD). Yet, as with all antidepressant treatments including electroconvulsive therapy (ECT), not all TRD patients adequately respond, and we are presently unable to a priori predict who will respond or not respond to ketamine. Therefore, antidepressant treatment response biomarkers to ketamine have been a major focus of research for over a decade. In this article, we review the evidence in support of treatment response biomarkers, with a particular focus on genetics, functional magnetic resonance imaging, and neurophysiological studies, i.e. electroencephalography and magnetoencephalography. The studies outlined here lay the groundwork for replication and dissemination.

scholarly journals Comparative efficacy between ketamine, memantine, riluzole and d-cycloserine in patients diagnosed with drug resistant depression: a meta-analysis

2019 ◽  
Vol 8 (6) ◽  
pp. 1132
Author(s):  
Nishita H. Darji ◽  
Devang A. Rana ◽  
Supriya D. Malhotra
Keyword(s):  
Rating Scale ◽  
Meta Analysis ◽  
Random Effect ◽  
Random Effect Model ◽  
Fixed Effect ◽  
P Value ◽  
Drug Resistant ◽  
Effect Model ◽  
Resistant Depression ◽  
Glutamate Modulators

Background: Glutamate modulators are having immense potential and are newer entities for treating drug resistant depression. The objectives were to generate statistical evidence on basis of existing data of ketamine, memantine, riluzole and d-cycloserine in resistant depression.Methods: A total of 14 RCTs following PRISMA guidelines and matching inclusion and exclusion criteria were collected of ketamine (5), memantine (3), riluzole (2) and d-cycloserine (4) vs placebo in drug resistant depression. Only RCTs with primary diagnosis of drug resistant depression (Previously on two standard antidepressant therapy) were included. Studies with treatment response rate, 50% reduction in total score of the depression rating scale-Montgomery-Åsberg Depression Rating Scale or the Hamilton Depression Rating Scale or Beck Depression Inventory was chosen as clinical outcome measure. RevMan 5.3 software was used for the analysis.Results: In ketamine group using random effect model SMD was 2.122 (95% CI 0.659-3.584). P-value was statistically significant (random effect p <0.005 and in fixed effect <0.001). In memantine group, using random effect model -0.963 was SMD and (95% CI -1.958-0.0324). P-value was <0.001, significant in fixed effect. In riluzole group, SMD was -0.564 with (95% CI -3.927-2.799) in random effect. P-value was 0.741. In d-cycloserine group SMD was 0.316 with (95% CI -1.252-1.885) in random effect. P-value was 0.690.Conclusions: Ketamine showed best efficacy followed by memantine. Riluzole and DCS as such have no efficacy although its acts by same glutamate pathway. More molecular based research is required in use of glutamate modulators in resistant depression.

Glutamate modulators for treatment of schizophrenia

2019 ◽  
Vol 15-16 ◽  
pp. 1-12
Author(s):  
Naista Zhand ◽  
David G. Attwood ◽  
Philip D. Harvey
Keyword(s):  
Glutamate Modulators

Identification of Adverse Drug Reactions by Evaluation of a Prescription Database, Demonstrated for “Risk of Bleeding”

2005 ◽  
Vol 44 (05) ◽  
pp. 697-703 ◽  
Author(s):  
J. Westendorf ◽  
R. Diebow ◽  
M. Kieser ◽  
W. Gaus
Keyword(s):  
Adverse Drug Reactions ◽  
Cholinesterase Inhibitors ◽  
Risk Profile ◽  
Bleeding Complications ◽  
Prescription Database ◽  
Drug Reactions ◽  
Risk Of Bleeding ◽  
Antidementia Drugs ◽  
Glutamate Modulators ◽  
Prescription Databases

Summary Objective: Information about adverse drug reactions plays an important role when assessing the benefit/risk profile of a drug. Identifying rare adverse drug reactions, however, is a difficult task. This paper illustrates the advantages of using a prescription database for this purpose. Methods: The mediplus® database used in our analysis covered data from 320,644 outpatients observed between July 1999 and June 2002. The example of bleeding complications during intake of antidementia drugs is used to illustrate this approach. The comparison of cohorts and subgroups is nearly always a problem in surveys. For our analyses we considered a set of patients who had taken a selected medication for a certain period of time and compared the frequency of adverse events with those occurring when the same patients did not take this medication. Hence, the comparison with versus without a certain medication is based on the same set of patients as in a cross-over study. Results: Our evaluations indicate that the rate of bleeding complications is low when taking any of the widely used antidementia drugs, glutamate modulators, cholinesterase inhibitors, calcium antagonists or the phytomedicine Ginkgo biloba. Conclusion: Basing the comparison of the rates of complications during periods with and without intake of a certain drug on the same set of patients may be a useful tool for assessing adverse drug reactions from data reported in prescription databases.

Novel dipyrazoles acting as glutamate modulators

2007 ◽  
Vol 17 (12) ◽  
pp. 1489-1493 ◽  
Author(s):  
Pierre Francotte ◽  
Pascal de Tullio ◽  
Bernard Pirotte
Keyword(s):  
Glutamate Modulators

scholarly journals Efficacy of Glutamate Modulators in Tic Suppression: A Double-Blind, Randomized Control Trial of D-serine and Riluzole in Tourette Syndrome

2015 ◽  
Vol 52 (6) ◽  
pp. 629-634 ◽  
Author(s):  
Monica E. Lemmon ◽  
Marco Grados ◽  
Tina Kline ◽  
Carol B. Thompson ◽  
Syed F. Ali ◽  
...  
Keyword(s):  
Tourette Syndrome ◽  
Randomized Control Trial ◽  
Double Blind ◽  
Tic Suppression ◽  
Randomized Control ◽  
Glutamate Modulators

scholarly journals Glutamate modulators as novel interventions for mood disorders

2005 ◽  
Vol 27 (3) ◽  
pp. 243-248 ◽  
Author(s):  
Sanjay J Mathew ◽  
Kathryn Keegan ◽  
Lisa Smith
Keyword(s):  
Mood Disorders ◽  
Ampa Receptor ◽  
Clinical Investigation ◽  
Nmda Receptor Antagonist ◽  
Open Label ◽  
Vesicular Release ◽  
Glutamate Modulators ◽  
Neuroprotective Function ◽  
Neurotrophic Signaling ◽  
Ampa Receptor Potentiators

Recent evidence suggests that critical molecules in neurotrophic signaling cascades are long-term targets for currently available monoaminergic antidepressants. As chronic and severe mood disorders are characterized by impairments in neuronal resilience, pharmacological strategies that subserve a neuroprotective function might alter disorder pathophysiology and modify disease progression. Several promising approaches involve modulation of the glutamate neurotransmitter system, via post-synaptic receptor blockade or potentiation and presynaptic vesicular release inhibition. A focused review of the extant scientific literature was conducted, with a discussion of 3 compounds or classes of drugs currently undergoing clinical investigation: ketamine, riluzole, and AMPA receptor potentiators. Recent investigations in mood disordered patients suggest that the NMDA receptor antagonist ketamine might demonstrate rapid antidepressant properties. Riluzole has been shown to reverse glutamate-mediated impairments in neuronal plasticity and to stimulate the synthesis of brain derived neurotrophic factor. Open-label trials in treatment-resistant depression have yielded promising results. Likewise, AMPA receptor potentiators favorably impact neurotrophic factors as well as enhance cognition. CONCLUSIONS: Pharmacological approaches that modulate components of the glutamate system offer novel targets for severe, recurrent mood disorders. Controlled studies are necessary.

Glutamate modulators as potential therapeutic drugs in schizophrenia and affective disorders

2013 ◽  
Vol 263 (5) ◽  
pp. 367-377 ◽  
Author(s):  
Kenji Hashimoto ◽  
Berend Malchow ◽  
Peter Falkai ◽  
Andrea Schmitt
Keyword(s):  
Affective Disorders ◽  
Therapeutic Drugs ◽  
Glutamate Modulators

scholarly journals Analgesic and Antidepressant Effects of the Clinical Glutamate Modulators Acetyl-L-Carnitine and Ketamine

2021 ◽  
Vol 15 ◽  
Author(s):  
Ulderico Freo ◽  
Viola Brugnatelli ◽  
Fabio Turco ◽  
Gastone Zanette
Keyword(s):  
Chronic Pain ◽  
Depressive Disorders ◽  
Day Surgery ◽  
Brain Regions ◽  
Stressful Events ◽  
Prefrontal Cortical ◽  
Post Operative Pain ◽  
Antidepressant Effects ◽  
Sparing Effect ◽  
Glutamate Modulators

Pain and depression are leading causes of disability and of profound social and economic burden. Their impact is aggravated by their chronicity and comorbidity and the insufficient efficacy of current treatments. Morphological and functional metabolism studies link chronic pain and depressive disorders to dysfunctional neuroplastic changes in fronto-limbic brain regions that control emotional responses to painful injuries and stressful events. Glutamate modulators are emerging new therapies targeting dysfunctional brain areas implicated in the generation and maintenance of chronic pain and depression. Here, we report the effects of two clinically approved glutamate modulators: acetyl-L-carnitine (ALCAR) and S, R(±)ketamine (KET). ALCAR is a natural neurotrophic compound currently marketed for the treatment of neuropathies. KET is the prototypical non-competitive antagonist at N-methyl-D-aspartate glutamate receptors and a clinically approved anesthetic. Although they differ in pharmacological profiles, ALCAR and KET both modulate aminergic and glutamatergic neurotransmissions and pain and mood. We assessed in rats the effects of ALCAR and KET on cerebral metabolic rates for glucose (rCMRglc) and assessed clinically the effects of ALCAR in chronic pain and of KET in post-operative pain. ALCAR and KET increased rCMRglc at similar degrees in prefrontal, somatosensory, and cingulate cortices, and KET increased rCMRglc at a different, much larger, degree in limbic and dopaminergic areas. While rCMRglc increases in prefrontal cortical areas have been associated with analgesic and antidepressant effects of ALCAR and KET, the marked metabolic increases KET induces in limbic and dopaminergic areas have been related to its psychotomimetic and abuse properties. In patients with chronic neuropathic pain, ALCAR (1,000 mg/day) yielded to a fast (2 weeks) improvement of mood and then of pain and quality of life. In day-surgery patients, KET improved dischargeability and satisfaction. In obese patients undergoing bariatric surgery, a single, low dose of KET (0.5 mg/kg) at induction of anesthesia determined a very fast (hours) amelioration of post-operative depression and pain and an opioid-sparing effect. These findings indicate that ALCAR and KET, two non-selective glutamate modulators, still offer viable therapeutic options in comorbid pain and depression.

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