The effect of N-acetylcysteine (NAC) on human cognition – A systematic review

Skvarc, David; Dean, Olivia; Byrne, Linda K.; Gray, Laura J.; Lane, Stephen; Lewis, Matthew; Fernandes, Brisa S.; Berk, Michael; Marriott, Andrew

doi:10.1016/j.neubiorev.2017.04.013

Cited by 84 publications

(53 citation statements)

References 130 publications

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“…Another study suggested that regional changes in frontal lobe metabolism on FDG-PET is associated with specific changes in memory in MS patient (41). It is also interesting to note that a systematic review of the effects of NAC suggest that it may generally help improve cognitive performance in a variety of conditions (42). While there were no MS studies in this meta-analysis, the suggestive efficacy signal in conditions like Alzheimer's Disease lends support to the construct of NAC improving oxidative stress pathways resulting in improved neuronal function.…”

Section: Discussionmentioning

confidence: 99%

N-acetyl Cysteine Administration Is Associated With Increased Cerebral Glucose Metabolism in Patients With Multiple Sclerosis: An Exploratory Study

et al. 2020

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Background: Multiple Sclerosis (MS) is an autoimmune disease marked by progressive neurocognitive injury. Treatment options affording neuroprotective effects remain largely experimental. The purpose of this proof of concept study was to explore the effects of N-acetyl-cysteine (NAC) on cerebral glucose metabolism (CMRGlu) and symptoms in patients with multiple sclerosis (MS). Methods: Twenty-four patients with MS were randomized to either NAC plus standard of care, or standard of care only (waitlist control). The experimental group received NAC intravenously once per week and orally the other 6 days. Patients in both groups were evaluated at baseline and after 2 months (of receiving the NAC or waitlist control period) with an integrated Position Emission Tomography (PET)/ Magnetic Resonance Imaging (MRI) scanner, using 18F Fluorodeoxyglucose (FDG) to measure cerebral glucose metabolism. Following imaging evaluation at 2 months, subjects initially attributed to the standard of care arm were eligible for treatment with NAC. Clinical and symptom questionnaires were also completed initially and after 2 months. Results: The FDG PET data showed significantly increased cerebral glucose metabolism in several brain regions including the caudate, inferior frontal gyrus, lateral temporal gyrus, and middle temporal gyrus (p < 0.05) in the MS group treated with NAC, as compared to the control group. Self-reported scores related to cognition and attention were also significantly improved in the NAC group as compared to the control group. Conclusions: The results of this study suggest that NAC positively affects cerebral glucose metabolism in MS patients, which is associated with qualitative, patient reported improvements in cognition and attention. Larger scale studies may help to determine the clinical impact of NAC on measures of functioning over the course of illness, as well as the most effective dosage and dosage regimen.

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Section: Discussionmentioning

confidence: 99%

N-acetyl Cysteine Administration Is Associated With Increased Cerebral Glucose Metabolism in Patients With Multiple Sclerosis: An Exploratory Study

et al. 2020

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“…A systematic review of clinical trials involving NAC support its potential role in managing various psychiatric conditions including but not limited to depression, bipolar disorder and schizophrenia (Deepmala et al, ). Further analysis of the literature suggests NAC could have a positive impact on human cognition, though further research is required (Skvarc et al, ). A preliminary study of patients with psychosis (n = 58) found an association between NAC treatment and improved working memory after 24 weeks (Rapado‐Castro et al, ).…”

Section: Resultsmentioning

confidence: 99%

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

Robertson

Coronado

Sethi

et al. 2019

Early Intervention Psych

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Aim: Neuropsychiatric disorders including depression, bipolar and schizophrenia frequently exhibit a neuroprogressive course from prodrome to chronicity. There are a range of agents exhibiting capacity to attenuate biological mechanisms associated with neuroprogression. This review will update the evidence for putative neuroprotective agents including clinical efficacy, mechanisms of action and limitations in current assessment tools, and identify novel agents with neuroprotective potential.Method: Data for this review were sourced from online databases PUBMED, Embase and Web of Science. Only data published since 2012 were included in this review, no data were excluded based on language or publication origin.Results: Each of the agents reviewed inhibit one or multiple pathways of neuroprogression including: inflammatory gene expression and cytokine release, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophin dysregulation and apoptotic signalling. Some demonstrate clinical efficacy in preventing neural damage or loss, relapse or cognitive/functional decline. Agents include: the psychotropic medications lithium, second generation antipsychotics and antidepressants; other pharmacological agents such as minocycline, aspirin, cyclooxygenase-2 inhibitors, statins, ketamine and alpha-2-delta ligands; and others such as erythropoietin, oestrogen, leptin, N-acetylcysteine, curcumin, melatonin and ebselen.Conclusions: Signals of evidence of clinical neuroprotection are evident for a number of candidate agents. Adjunctive use of multiple agents may present a viable avenue to clinical realization of neuroprotection. Definitive prospective studies of neuroprotection with multimodal assessment tools are required.

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“…Auf dieser Grundlage baut ein vielversprechender präventiver Behandlungsansatz auf, welcher die Fehlfunktionen des Redoxsystems und die daraus folgenden Myelinisierungsdefizite zu korrigieren versucht. Konkrete Ziele dieser Behandlungen sind der Abbau von oxidativem Stress und die Regeneration der oxidativen Homöostase (14,15).…”

Section: Discussionunclassified

Prävention einer ersten psychotischen Episode

Schultz¹,

Wasserthal²,

Kloss³

et al. 2018

Nervenheilkunde

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Zusammenfassung Gegenstand und Ziel: Psychotische Störungen gehören aufgrund ihres frühen Beginns und ihren langfristigen Konsequenzen zu den teuersten psychischen Erkrankungen in Europa. Prävention könnte die gesellschaftlichen Kosten und die immense Belastung für Patienten und Familien signifikant reduzieren. Neurobiologische Befunde deuten auf eine glutamaterge Dysfunktion und ein Redoxungleichgewicht in der Pathophysiologie der Schizophrenie. Wir vermuten, dass Interventionen, die auf soziale Funktionen und glutamaterge /oxidative Signalwege abzielen, die Übergangsraten signifikant reduzieren würden. Material und Methoden: Unsere Studie ist eine randomisierte, placebokontrollierte 18-monatige Studie (6-Monate Intervention; 12 Monate Nachuntersuchung) mit 200 Probanden, die ein klinisch erhöhtes Risiko für Psychosen haben. Wir werden in einem 2x2-faktoriellen Design die präventiven Effekte einer kognitiv-behavioralen und sozial-kognitiven Intervention (IPPI) mit einer pharmakologischen Intervention mit einem pro-glutamatergen, neuroprotektiven Medikament (N-Acetylcystein) vergleichen. Ergebnisse und klinische Relevanz: Die Ergebnisse dieser Studie sollen zu neuen, gut verträglichen präventiven Interventionen führen.

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The effect of N-acetylcysteine (NAC) on human cognition – A systematic review

Cited by 84 publications

References 130 publications

N-acetyl Cysteine Administration Is Associated With Increased Cerebral Glucose Metabolism in Patients With Multiple Sclerosis: An Exploratory Study

N-acetyl Cysteine Administration Is Associated With Increased Cerebral Glucose Metabolism in Patients With Multiple Sclerosis: An Exploratory Study

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

Prävention einer ersten psychotischen Episode

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