CommentaryTranslating the Rosetta Stone of N-Acetylcysteine
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Cited by (17)
Mitochondrial dysfunction in bipolar disorder: Evidence, pathophysiology and translational implications
2016, Neuroscience and Biobehavioral ReviewsCitation Excerpt :The restoration of the electron chain transfer process by NAC has been attributed at least in part to the redox-state of the thiols groups in the mitochondrial complex because thiol groups are essential for respiratory mitochondrial enzymes (Dupuis et al., 1991; Zhang et al., 1990). Overall, NAC has promise as an add-on drug in the management of psychiatric disorders (Berk et al., 2011a; Dean et al., 2011, 2012). Berk et al. (2008) conducted a randomized, placebo-controlled trial of NAC in BD sponsored by the Stanley Medical Research Institute.
Pharmacological targeting of redox regulation systems as new therapeutic approach for psychiatric disorders: A literature overview
2016, Pharmacological ResearchCitation Excerpt :However, the study failed to show any significant differences between the two groups in both the frequency and latency of new episodes of either depression or mania [64]. In another study, NAC also failed to improve alterations of cognitive functions in bipolar patients, with respect to placebo [126]. Subsequent studies focused specifically on depressive symptoms of bipolar disorders.
Multiprobe molecular imaging of an NMDA receptor hypofunction rat model for glutamatergic dysfunction
2016, Psychiatry Research - NeuroimagingCitation Excerpt :Activated microglia stimulate astrocytes and these astrocytes respond by releasing excessive glutamate that binds to mGluR5 receptors on neurons and induces neuroinflammation through neurotoxicity (Zantomio et al., 2015). N-Acetyl-cysteine (NAc) shows beneficial effects in schizophrenia-like pathology and it has previously been postulated that the main benefits would be through restoration of depleted GSH levels-which normalizes microglial glutamate release and stimulates the NMDAR input to inhibitory GABA-ergic interneurons through its redox modulatory site, as illustrated in Fig. 1A(11)-and direct scavenging of free radicals (Berk et al., 2013; Dean et al., 2012). Additionally, NAc activates the cysteine-glutamate antiporter, thereby increasing the extrasynaptic glutamate release, hence reducing the glutamate release in the synaptic cleft through stimulation of its reuptake via mGluR2/3.
Towards stage specific treatments: Effects of duration of illness on therapeutic response to adjunctive treatment with N-acetyl cysteine in schizophrenia
2015, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :A trial of N-acetyl cysteine (NAC), a glutathione precursor, as an adjunctive treatment in schizophrenia has shown an attenuation of negative symptoms, general symptoms and overall functioning after 24 weeks of treatment (Berk et al., 2008a,b) providing some support for a role of oxidative stress in schizophrenia. It is likely that NAC is exerting benefits beyond being a precursor to the GSH however, as it has properties that modulate glutamatergic, neurotropic and inflammatory pathways (Berk et al., 2013; Dean et al., 2012). Progressive changes in these pathways have been thought to underpin the staged process of neuroprogression observed in the disorder, and interact with oxidative factors.
The promise of N-acetylcysteine in neuropsychiatry
2013, Trends in Pharmacological SciencesCitation Excerpt :The principal victories in biological psychiatry have arisen from the quest to reverse engineer serendipitous clinical findings. Exploring the biological effects of tricyclics, antipsychotics, and lithium have, respectively, led to elucidating the role of monoamines in depression, dopamine in schizophrenia, and second messenger systems in bipolar disorder [2]. In a similar vein, NAC provides a dual opportunity, first as a novel therapy, and second as a key to unlocking the pathophysiology of targeted disorders.