Quercetin as an Augmentation Agent in Schizophrenia

Schwartz, Darren

doi:10.1097/jcp.0000000000000498

Cited by 10 publications

(6 citation statements)

References 20 publications

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“…It also improves the behavioral impairments in schizophrenic models [ 169 ]. A case study report by Schwartz suggests that quercetin can be effectively used to boost antipsychotic therapy [ 170 ].…”

Section: Honey and Neurological Disordersmentioning

confidence: 99%

Potential Therapeutic Benefits of Honey in Neurological Disorders: The Role of Polyphenols

et al. 2022

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Honey is the principal premier product of beekeeping familiar to Homo for centuries. In every geological era and culture, evidence can be traced to the potential usefulness of honey in several ailments. With the advent of recent scientific approaches, honey has been proclaimed as a potent complementary and alternative medicine for the management and treatment of several maladies including various neurological disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis, etc. In the literature archive, oxidative stress and the deprivation of antioxidants are believed to be the paramount cause of many of these neuropathies. Since different types of honey are abundant with certain antioxidants, primarily in the form of diverse polyphenols, honey is undoubtedly a strong pharmaceutic candidate against multiple neurological diseases. In this review, we have indexed and comprehended the involved mechanisms of various constituent polyphenols including different phenolic acids, flavonoids, and other phytochemicals that manifest multiple antioxidant effects in various neurological disorders. All these mechanistic interpretations of the nutritious components of honey explain and justify the potential recommendation of sweet nectar in ameliorating the burden of neurological disorders that have significantly increased across the world in the last few decades.

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Section: Honey and Neurological Disordersmentioning

confidence: 99%

Potential Therapeutic Benefits of Honey in Neurological Disorders: The Role of Polyphenols

et al. 2022

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“…Quercetin [160,161] (NCT04063124), Ethyl eicosopentanoic acid [76,145] Genistein [162,163] (NCT01982578) Glucose-dependent insulionotropic polypeptide [143] Andrographolide [164] Alpha-lipoic acid [144] (NCT03788759) CXA-10 [165] L-arginine [142] (NCT04054973)…”

Section: Treatment-engagement and Stratification Markers (Gsh) For Antioxidant Trialsmentioning

confidence: 99%

“…An exciting clinical utility of prospectively identifying patients with GSH-deficit is the therapeutic possibility of correcting it. A number of compounds with the potential to correct the effects of GSH deficit are in the pipeline ( Table 2 ) [ 44 , 76 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 ]. Of these, N-acetylcysteine has been shown to improve cognition and negative symptoms (6 RCTs) [ 172 ], though the effect size is modest.…”

Section: Treatment-engagement and Stratification Markers (Gsh) For Antioxidant Trialsmentioning

confidence: 99%

“…Reliable characterisation of the GSH-deficit phenotype is critical in this regard. Furthermore, while the antioxidant pipeline is promising [ 44 , 76 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 ], reversing cognitive/negative symptoms requires longer trials that are substantially difficult to complete. We need reliable markers of biological efficacy that indicate engagement of the mechanistic target; this will help overcome several obstacles in clinical translation (e.g., targeted in vivo assay, dose finding, estimating trial duration, understanding placebo response).…”

Section: Treatment-engagement and Stratification Markers (Gsh) For Antioxidant Trialsmentioning

confidence: 99%

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Is There a Glutathione Centered Redox Dysregulation Subtype of Schizophrenia?

et al. 2021

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Schizophrenia continues to be an illness with poor outcome. Most mechanistic changes occur many years before the first episode of schizophrenia; these are not reversible after the illness onset. A developmental mechanism that is still modifiable in adult life may center on intracortical glutathione (GSH). A large body of pre-clinical data has suggested the possibility of notable GSH-deficit in a subgroup of patients with schizophrenia. Nevertheless, studies of intracortical GSH are not conclusive in this regard. In this review, we highlight the recent ultra-high field magnetic resonance spectroscopic studies linking GSH to critical outcome measures across various stages of schizophrenia. We discuss the methodological steps required to conclusively establish or refute the persistence of GSH-deficit subtype and clarify the role of the central antioxidant system in disrupting the brain structure and connectivity in the early stages of schizophrenia. We propose in-vivo GSH quantification for patient selection in forthcoming antioxidant trials in psychosis. This review offers directions for a promising non-dopaminergic early intervention approach in schizophrenia.

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“…The findings of Fan and colleagues are especially notable given a recent publication describing two case studies in which augmenting conventional antipsychotic treatments with quercetin improved therapeutic outcomes in schizophrenia patients [ 7 ]. Together, these provide early evidence in both rodents and humans for a novel, unexplored treatment that targets the interplay between excitation and inhibition in the PFC.…”

mentioning

confidence: 99%