Antioxidant N-acetylcysteine during Childhood to Protects Against Psychiatric Disorders

Apart from several other environmental or genetic factors, oxidative stress (OS) leading to free radical attack on neural cells have been in scientific studies for some time showing its calamitous role in neuro-degeneration. A new study published in Elsevier (Biological Psychiatry, Volume 73, Issue 6) shows that OS due to lack of antioxitants can lead to impaired parvalbumin neurons in the brains of mice that were stressed when they were young leading to permanent impairments throughout their life.

Interestingly, the same stresses applied to adults had no effect on their parvalbumin neurons. Most strikingly, mice treated with the antioxidant N-acetylcysteine, from before birth and onwards, were fully protected against these negative consequences on parvalbumin neurons.

The activity of Parvalbumin neurons is critical for proper cognitive and emotional functioning. Parvalbumin is a subtype of Gamma-aminobutyric acid (GABA) neuron which is shown to be particularly vulnerable to oxidative stress. These oxidative stresses can be due to infections, inflammations, traumas or psychosocial stress occurring during typical brain development, meaning that at-risk subjects are particularly exposed during childhood and adolescence, but not once they reach adulthood.

Dr. Kim Do from the Center for Psychiatric Neurosciences of Lausanne University in Switzerland says “To give an antioxidant from childhood on to carriers of a genetic vulnerability for schizophrenia could reduce the risk of emergence of the disease.”

The study provides a major development in treatment of psychiatric disorders like schizophrenia, bipolar disorder and depression. It concludes that parvalbumin neurons may be protected from this effect by N-acetylcysteine, also known as Mucomyst, a medication commonly prescribed to protect the liver against the toxic effects of acetaminophen (Tylenol) overdose.