N-Acetylcysteine as an Adjunct to Risperidone for Treatment of Negative Symptoms in Patients With Chronic Schizophrenia

Farokhnia, Mehdi; Azarkolah, Anita; Adinehfar, Forod; Khodaie‐Ardakani, Mohammad‐Reza; Hosseini, Saeed; Yekehtaz, Habibeh; Tabrizi, Mina; Rezaei, Farzin; Salehi, Bahman; Sadeghi, Seyed-Mohammad-Hossein; Moghadam, Marzieh; Gharibi, Fardin; Mirshafiee, Omid; Akhondzadeh, Shahin

doi:10.1097/wnf.0000000000000001

Cited by 129 publications

(96 citation statements)

References 37 publications

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“…152 Two additional studies also demonstrate that chronic patients improved with supplemental NAC, particularly in their negative symptoms. 153,154 Moreover, NAC normalized neuronal activity and connectivity and improved MMN, 155 an auditory-related, NMDAdependent evoked potential typically impaired in SZ. 156 Although not performed during development, these studies can be considered as a proof-of-concept, pointing to the efficacy of an antioxidant and possibly favoring the closure of a pathological CP.…”

Section: Outlook For Preventive Developmental Therapiesmentioning

confidence: 92%

Targeting Oxidative Stress and Aberrant Critical Period Plasticity in the Developmental Trajectory to Schizophrenia

Q.¹,

Cuénod²,

Hensch

2015

SCHBUL

138

111

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Schizophrenia is a neurodevelopmental disorder reflecting a convergence of genetic risk and early life stress. The slow progression to first psychotic episode represents both a window of vulnerability as well as opportunity for therapeutic intervention. Here, we consider recent neurobiological insight into the cellular and molecular components of developmental critical periods and their vulnerability to redox dysregulation. In particular, the consistent loss of parvalbumin-positive interneuron (PVI) function and their surrounding perineuronal nets (PNNs) as well as myelination in patient brains is consistent with a delayed or extended period of circuit instability. This linkage to critical period triggers (PVI) and brakes (PNN, myelin) implicates mistimed trajectories of brain development in mental illness. Strategically introduced antioxidant treatment or later reinforcement of molecular brakes may then offer a novel prophylactic psychiatry.

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Section: Outlook For Preventive Developmental Therapiesmentioning

confidence: 92%

Targeting Oxidative Stress and Aberrant Critical Period Plasticity in the Developmental Trajectory to Schizophrenia

Q.¹,

Cuénod²,

Hensch

2015

SCHBUL

138

111

View full text Add to dashboard Cite

show abstract

“…Clinical trials demonstrated beneficial effects of N-acetylcysteine [117][118][119][120][121], omega-3 fatty acids [122,123] and vitamins E and C [123] in the treatment of schizophrenia. Furthermore, these studies seem to suggest that antioxidant treatment supports positive outcomes in the early stage of schizophrenia.…”

Section: Reversed [80]mentioning

confidence: 99%

Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism

Smaga

Niedzielska

Gawlik

et al. 2015

Pharmacological Reports

216

115

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The pathophysiology of psychiatric diseases, including depression, anxiety, schizophrenia and autism, is far from being fully elucidated. In recent years, a potential role of the oxidative stress has been highlighted in the pathogenesis of neuropsychiatric disorders. A body of clinical and preclinical evidence indicates that psychiatric diseases are characterized by higher levels of oxidative biomarkers and with lower levels of antioxidant defense biomarkers in the brain and peripheral tissues. In this article, we review current knowledge on the role of the oxidative stress in psychiatric diseases, based on clinical trials and animal studies, in addition, we analyze the effects of drug-induced modulation of oxidative balance and explore pharmacotherapeutic strategies for oxidative stress reduction.

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“…Studies have concentrated on medications such as N-acetylcysteine (NAC), ginkgo biloba extracts (EGb), ω-3 fatty acids, and vitamins C and E. Farokhnia, et al [17] found that a combination of antipsychotic medications with NAC significantly improved schizophrenics negative symptoms while no significant effects were found in improving either positive symptoms or general psychopathology symptoms (based on the changes of the PANSS total scores and its three subscale scores). Jingfeng Qi, et al [18] found, in a psychiatric study, that ω-3 fatty acids increased antioxidant enzyme levels and alleviated oxidative stress in the brain, was synergistic with antipsychotic medications, improved PANSS total scores, and separately improved schizophrenic symptoms.…”

Section: Effects Of Antioxidants On Schizophreniamentioning

confidence: 99%

Cognitive Impairment of Chronic Alcohol Dependence and Its Relationship with Prefrontal Cortex

2017

J Psychiatry Brain Sci.

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Many studies show that oxidative stress is a pathophysiological mechanism of schizophrenia. Elevated oxidative stress levels and the damage to the antioxidant defense system can observed in early schizophrenia. High oxidation levels damage lipids, proteins, nucleic acids and other tissues. Antioxidant defense system imbalance has been observed in both neuroleptic-naïve first-episode schizophrenics and chronic schizophrenics being treated with medication and indicates the presence of oxidative stress in schizophrenia.Antipsychotic drugs also exert certain impacts on oxidative stress while improving the schizophrenia clinical symptoms. Antioxidants synergistically improve schizophrenia clinical symptoms. A combination regime of antipsychotic drugs and antioxidants is a potentially effective treatment strategy for schizophrenia.Keywords: Schizophrenia; Oxidative stress; Antioxidant defense system; Antioxidants.Schizophrenia is a common, serious mental illness, usually associated with, among other things, disordered perceptions, thoughts, emotions, volition and behavior. Major symptoms include positive symptoms (e.g. delusions or hallucinations), negative symptoms (i.e. affective flattening, alogia, or avolition) and cognitive dysfunction. The precise etiology of the disease remain unclear and both genetic and environmental factors appear to be involved. Recently scholars and researchers have begun to study the effect of oxidative stress on schizophrenia pathophysiology and it is thought to be involved in schizophrenia generation and development. This study reviews, and summarizes, schizophrenia pathogenesis, and oxidative stress medication therapy. Oxidative stress explained first, followed by a discussion of its relationship to schizophrenia. It then discusses http://jpbs.qingres.com

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N-Acetylcysteine as an Adjunct to Risperidone for Treatment of Negative Symptoms in Patients With Chronic Schizophrenia

Abstract: NAC add-on therapy showed to be a safe and effective augmentative strategy for alleviating negative symptoms of schizophrenia.

Cited by 129 publications

References 37 publications

Targeting Oxidative Stress and Aberrant Critical Period Plasticity in the Developmental Trajectory to Schizophrenia

Targeting Oxidative Stress and Aberrant Critical Period Plasticity in the Developmental Trajectory to Schizophrenia

Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism

Cognitive Impairment of Chronic Alcohol Dependence and Its Relationship with Prefrontal Cortex

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