Kynurenic Acid: Does It Bar Schizophrenics From Making Executive Decisions?

Foreword: Not when the brain compound is within its specified limits; inability in schizophrenics to handle day-to-day problems occurs when its levels get elevated in their brains. It is a study by Dr. John P. Bruno (Professor of Psychology, Psychiatry and Neuroscience; Ohio State University), who also mentioned the reformatory measures as important supplements for the anti-psychotic medicines administered normally for treating the most resistant indications of cognitive impairment disorders.

Schizophrenia and its effects on an individual: Schizophrenia involves both hallucination and delusion, which further reduces the cognitive flexibility in individuals suffering from the disorder, which again stops individuals from adjusting their thought processes to changing circumstances. It's only through a much-lengthy process they can set their goals or plan ways to achieve the goals.

The role of Kynurenic acid: KYNA is a neuro-active component of the human brain and is produced when the amino acid L-tryptophan is normally metabolized. Its chief function is to act as an anti-excito-toxic and an anticonvulsant by resisting the excitatory amino acids from binding to the following receptors, namely:

Glycine site of the NMDA receptor.

Alpha-7 nicotinic acetylcholine (a neurotransmitter involved in the brains chemical communication system and a derivative of choline; released at the ends of nerve fibers in the somatic and parasympathetic nervous systems) receptor.

N.B. An action contrary to 5-hydroxyindoleacetic acid, another tryptophan metabolite.

iii. As a ligand (an atom/molecule/radical/ion that forms a complex around a central atom) for GPR35, the orphan receptor for coupled G protein.

As a result, KYNA influences certain vital neuro-physiologic and neuro-pathologic processes and found usage in treating a number of neurobiological disorders.

When KYNA is present in excess: Increased KYNA levels have been noticed to initiate the pathogenesis of schizophrenia by suppressing the alpha-7 receptors, resulting in the compound's interference as well with other chemical processes governing cognitive abilities like concentrating and thinking strategically in a commutative environment.

N.B. KYNA is also found in excess in victims of tick-borne encephalitis and illnesses involving immunodeficiency. Studies revealed the increased levels to initiate both confusion and psychotic symptoms by influencing the effects of dopamine (a monoamine neurotransmitter found in the brain and essential for the normal functioning of the central nervous system) on the mid-brain and NMDA(N-methyl-D-aspartic acid)receptors. This links the hypothesis on dopamine to Schizophrenia's glutamate hypothesis. However, certain metabolic disorders like pyridoxine deficiency results in a deficit or complete absence of kynureninase to trigger the KYNA levels.

Usage of KYNA in treating Schizophrenia: So far, severe cognitive deficit treatments in schizophrenics involved the usage of anti-psychotic drugs, which brought forth the so-called positive symptoms (e.g. calming down) but did little to cure the conditions. So the experiments were ran on rats with medications that would elevate the KYNA levels in their brains and it was found they had trouble finding food under changing conditions. The research for enzymes that would inhibit the factors overproducing KYNA has begun; we might witness improved cognitive performances in Schizophrenics within sometime soon.