Schizophrenia, Carbonyl Stress and Carnosine
Volume 3 - Issue 4
Alan R Hipkiss*
- Aston Research Centre for Healthy Ageing (ARCHA), Aston University, United Kingdom
Received: December 03, 2019; Published: December 16, 2019
Corresponding author:Alan R Hipkiss, Aston Research Centre for Healthy Ageing (ARCHA), Aston University, Birmingham, United
Kingdom
DOI: 10.32474/OJNBD.2019.03.000168
Abstract
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Abstract
Recent research suggests that schizophrenia is associated with the development of an advanced aging phenotype (carbonyl
stress) and erythrocytes from schizophrenics also exhibit symptoms of cellular aging (increased levels of glycated proteins and
ubiquitinated proteins), possibly due to excessive glycolysis-induced methylglyoxal (MG) generation. The endogenous dipeptide
carnosine (beta-alanyl-L-histidine), which can delay cellular aging, suppress glycolysis and inhibit MG-induced protein glycation,
also exerts some beneficial effects towards schizophrenia. Carnosine is present in human erythrocytes and the olfactory bulb
(olfactory dysfunction is associated with schizophrenia). It is suggested that enhanced erythrocyte and olfactory carnosine levels
may be more therapeutic towards schizophrenia, if carnosine was also administered intra-nasally to avoid serum carnosinase
activity.
Keywords:Carnosine; glycation; methylglyoxal; erythrocyte; aging; nasal administration
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