N-acetylcysteine as a potentially useful medication to prevent conversion to schizophrenia in at-risk individuals

Abstract

Schizophrenia is a chronic and often severe psychotic disorder. Its causes include imbalances in mediators involved in neuroplasticity, apoptosis, cell resilience and dendritic arborization. Among these mediators, oxidative species are particularly relevant for the pathophysiology of the disease, and this is the rationale for experimental use of antioxidant medications, such as N-acetylcysteine (NAC). Onset of schizophrenia is usually preceded by a period of subtle and unspecific symptoms, the prodrome, in which preventive interventions could delay or even stop the progression to full-blown psychosis. In this article, we propose that NAC could be a useful medication to prevent evolution of schizophrenia in individuals at risk for psychosis.

Systematic review of N-acetylcysteine in the treatment of addictions

“…30 Chemical reactions related to the biosynthesis and metabolism of glutathione form the gamma-glutamyl cycle, which is also involved in the formation of DNA precursors. 31 The redox modulation produced by NAC may have an important protective effect on the brain, possibly reducing neuroprogression 32,33 associated with psychiatric diseases and with chronic use of potentially neurotoxic drugs. 34,35 This rationale is especially relevant in individuals at early stages of disease, when less structural brain damage is expected.…”

“…34,35 This rationale is especially relevant in individuals at early stages of disease, when less structural brain damage is expected. 33 The safety profile of NAC and its favorable tolerability highlight its potential for clinical use. 10 Being an over-thecounter medication, it could be useful in patients hesitant to accept conventional psychotropic medications.…”

Targeting the Inflammatory Pathway as a Therapeutic Tool for Major Depression

“…To our knowledge, curcumin has not been used in clinical trials for depression so far. NAC is a glutathione precursor that has been shown to be involved in oxidative homeostasis, dopamine modulations and to interact with several inflammatory markers [80]. Preclinical studies with these agents have yielded promising results so far, with evidence supporting an antidepressant-like effect in animal studies [81,82,83,84,85].…”

Impact of peripheral levels of chemokines, BDNF and oxidative markers on cognition in individuals with schizophrenia

“…Similarly, oxidative stress has been suggested to play a role in cognition, with oxidative species mediating conversion from mild cognitive impairment to Alzheimer's Disease (AD) (Pratico et al, 2002;Rodrigues et al, 2012). Cognition usually demands high levels of energy supply, making cognitive functions particularly vulnerable to mitochondrial dysfunction and oxidative imbalance (Asevedo et al, 2012;Brietzke et al, 2011;Wood et al, 2009). Inflammation has also been shown to impact cognition in some illnesses such as AD, Major Depressive Disorder and Bipolar Disorder (do Prado et al, 2013;Grassi-Oliveira et al, 2011).…”