Memantine in the prevention or alleviation of electroconvulsive therapy induces cognitive disorders: A placebo controlled trial

Abbasinazari, Mohammad; Adib-Eshgh, Ladan; Rostami, Azin; Beyraghi, Narges; Dabir, Shideh; Jafari, Reyhaneh

doi:10.1016/j.ajp.2015.04.002

Cited by 37 publications

(14 citation statements)

References 19 publications

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“…Finally, 5 RCTs were eligible and included in our systematic review. [ 6 , 10 , 11 , 20 , 21 ] The flow chart of the study selection process is shown in Figure 1 .…”

Section: Resultsmentioning

confidence: 99%

Prophylactic cognitive enhancers for improvement of cognitive function in patients undergoing electroconvulsive therapy

Niu¹,

Ye²,

You

et al. 2020

Medicine

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“…Finally, 5 RCTs were eligible and included in our systematic review. [ 6 , 10 , 11 , 20 , 21 ] The flow chart of the study selection process is shown in Figure 1 .…”

Section: Resultsmentioning

confidence: 99%

Prophylactic cognitive enhancers for improvement of cognitive function in patients undergoing electroconvulsive therapy

Niu¹,

Ye²,

You

et al. 2020

Medicine

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“…MEM is FDA-approved to treat dementia and preferentially blocks excessive NMDA receptor activity without disrupting normal activity (Johnson and Kotermanski 2005). Several lines of evidence suggest that MEM might have pro-cognitive effects in disorders other than dementias that are also characterized by cognitive deficits (Alizadeh et al 2015; Abbasinazari et al 2015). For example, MEM 20 mg acutely enhances cortical metabolic efficiency (Willenborg et al 2011) and improves neurocognition after brain injury, and these effects are strongly associated with increased left frontal and parietal lobe glucose metabolism (Kim et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Effects of acute memantine administration on MATRICS Consensus Cognitive Battery performance in psychosis: Testing an experimental medicine strategy

et al. 2016

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Rationale Pro-cognitive agents for chronic psychotic disorders (CPDs) might be detected via experimental medicine models, in which neural targets engaged by the drug predict sensitivity to the drug’s pro-cognitive effects. Objective This study aims to use an experimental medicine model to test the hypothesis that “target engagement” predicts pro-cognitive effects of the NMDA antagonist, memantine (MEM), in CPDs. Methods MATRICS Consensus Cognitive Battery (MCCB) performance was assessed in CPD (n = 41) and healthy subjects (HS; n = 41) in a double-blind, randomized cross-over design of acute (single dose) MEM (placebo vs. 10 or 20 mg p.o.). Measures of prepulse inhibition (PPI) and mismatch negativity previously reported from this cohort substantiated target engagement. Biomarkers predicting MEM neurocognitive sensitivity were assessed. Results Testing confirmed MCCB deficits associated with CPD diagnosis, age, and anticholinergic exposure. MEM (20 mg p.o.) reduced MCCB performance in HS. To control for significant test order effects, an “order-corrected MEM effect” (OCME) was calculated. In CPD subjects, greater age, positive MEM effects on PPI, and SNP rs1337697 (within the ionotropic NMDA receptor gene, GRIN3A) predicted greater positive OCME with 20 mg MEM. Conclusions An experimental medicine model to assess acute pro-cognitive drug effects in CPD subjects is feasible but not without challenges. A single MEM 20 mg dose had a negative impact on neurocognition among HS. In CPD patients, age, MEM effects on PPI, and rs1337697 predicted sensitivity to the neurocognitive effects of MEM. Any potential clinical utility of these predictive markers for pro-cognitive effects of MEM in subgroups of CPD patients cannot be inferred without a validating clinical trial.

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“…Add-on memantine 20 mg for 12 weeks in 64 inpatients with schizophrenia was significantly effective in improving the global functioning as well as their quality of life ( Omranifard et al, 2015 ). Finally, memantine 5–20 mg administered daily before electroconvulsive therapy (ECT) has been shown to improve cognitive performance after ECT ( Abbasinazari et al, 2015 , Alizadeh et al, 2015 ). Authors argued the possible role of glutamatergic system for ECT-associated cognitive impairments.…”

Section: Introductionmentioning

confidence: 99%

Kynurenine pathway and cognitive impairments in schizophrenia: Pharmacogenetics of galantamine and memantine

Koola

2016

Schizophrenia Research: Cognition

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The Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) project designed to facilitate the development of new drugs for the treatment of cognitive impairments in people with schizophrenia, identified three drug mechanisms of particular interest: dopaminergic, cholinergic, and glutamatergic. Galantamine is an acetylcholinesterase inhibitor and a positive allosteric modulator of the α7 nicotinic receptors. Memantine is an N-methyl-D-aspartate (NMDA) receptor antagonist. There is evidence to suggest that the combination of galantamine and memantine may be effective in the treatment of cognitive impairments in schizophrenia. There is a growing body of evidence that excess kynurenic acid (KYNA) is associated with cognitive impairments in schizophrenia. The α-7 nicotinic and the NMDA receptors may counteract the effects of kynurenic acid (KYNA) resulting in cognitive enhancement. Galantamine and memantine through its α-7 nicotinic and NMDA receptors respectively may counteract the effects of KYNA thereby improving cognitive impairments. The Single Nucleotide Polymorphisms in the Cholinergic Receptor, Nicotinic, Alpha 7 gene (CHRNA7), Glutamate (NMDA) Receptor, Metabotropic 1 (GRM1) gene, Dystrobrevin Binding Protein 1 (DTNBP1) and kynurenine 3-monooxygenase (KMO) gene may predict treatment response to galantamine and memantine combination for cognitive impairments in schizophrenia in the kynurenine pathway.

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Memantine in the prevention or alleviation of electroconvulsive therapy induces cognitive disorders: A placebo controlled trial

Cited by 37 publications

References 19 publications

Prophylactic cognitive enhancers for improvement of cognitive function in patients undergoing electroconvulsive therapy

Prophylactic cognitive enhancers for improvement of cognitive function in patients undergoing electroconvulsive therapy

Effects of acute memantine administration on MATRICS Consensus Cognitive Battery performance in psychosis: Testing an experimental medicine strategy

Kynurenine pathway and cognitive impairments in schizophrenia: Pharmacogenetics of galantamine and memantine

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