People with alcohol addiction lack key enzyme: Scientists

In people with alcohol dependence, the production of a key enzyme shuts down in brain cells and the deficiency leads to continued use of alcohol despite adverse consequences, say researchers.

The enzyme, PRDM2, has previously been studied in cancer research.

"But we didn't know that it has a function in the brain," said Markus Heilig, head of the Centre for Social and Affective Neuroscience (CSAN) at Linköping University in Sweden.

It has long been suspected that people with alcohol dependence have impaired function in the frontal lobes of the brain but the underlying biological mechanisms have not been known.

The research team, which includes researchers from both Linköping University and University of Miami, is the first to identify this molecular mechanism.

If frontal function is impaired, it is difficult for us to control our impulses.

A person with intact impulse control can walk past a bar on a warm day and think "a beer would be nice, but I can't have one now because I have to get back to work".

An alcoholic does not have sufficient impulse control to refrain, thinking: "It's hot and I'm thirsty".

"PRDM2 controls the expression of several genes that are necessary for effective signalling between nerve cells. When too little enzyme is produced, no effective signals are sent from the cells that are supposed to stop the impulse," Professor Heilig noted.

The team has shown that alcohol dependence in rats leads to a down-regulation of PRDM2 production, which, in turn, leads to disruption of impulse control.

When the researchers knocked out the production of PRDM2 in the frontal lobes of rats that were not dependent, they observed the same behaviour - impulse control was disrupted.

"Over the long term, we want to contribute to developing effective medicines, but over the short term the important thing is to do away with the stigmatisation of alcoholism," Professor Heilig added.

The discovery was published in the journal Molecular Psychiatry.

--IANS

na/bg