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Researchers from the University of Illinois in the United States have shown that some of these lasting changes result from epigenetic changes that alter the expression of a crucial protein for training and maintenance of neural connections in the amygdala, the part of the brain involved. in emotion, fear and anxiety.
Their findings, published in the journal Translational Psychiatry, are based on the badysis of postmortem human brain tissue.
Epigenetics refers to chemical modifications of DNA, RNA or specific proteins badociated with chromosomes, which alter the activity of genes without modifying the genes themselves.
Epigenetic changes are involved in the normal development of the brain, but they can be influenced by environmental or even social factors, such as alcohol and stress.
These types of epigenetic alterations have been linked to behavioral changes and diseases, said Subhash Pandey, a professor at the University of Illinois.
The researchers studied human post-mortal tonsillar tissue from the brain of 11 people who had started drinking copiously before the age of 21 or who had been drinking early; 11 people who started drinking seriously after the age of 21, called late drinkers; and 22 people with no history of drinking disorder.
The average age of death for those sampled was 58 years for those with no alcohol-related disorder; 55 years for early drinkers; and 59 for late drinkers.
Tonsils of individuals who were early drinkers had about 30% more of a molecule called BDNF-AS, a large non-coding RNA.
Usually, RNA is involved in the production of proteins from DNA, but the researchers claimed that this was not the case. BDNF-AS regulates a gene that produces a protein called BDNF.
This protein is a growth factor and is crucial for normal formation and maintenance of synapses throughout the brain.
When there is more BDNF-AS, there is less BDNF. The brain tissue of early drinkers contained 30 to 40% less BDNF than those without a history of alcohol-related disorders.
This reduction in BDNF was not observed in brain samples of late drinkers or people with no alcohol-related disorder.
Pandey believes that epigenetic modifications of BDNF-AS are the reason why BDNF is lower in tonsils, in people who started drinking early in life.
"BDNF is necessary for the normal development of the brain and the formation of connections between neurons," Pandey said.
"If levels are lowered due to alcohol exposure, the brain will not develop normally, and we see that in those brain samples where there are abnormalities in another synaptic gene, Arc , probably making abnormal connections between neurons, "he said.
The researchers found that the increase in BDNF-AS in early drinkers was due to a decrease in methylation of BDNF-AS.
Methylation is a type of epigenetic change in which a molecule containing a methyl group is added to another molecule and causes a change in gene expression.
It is thought that the decrease in methylation of BDNF-AS is due to early alcohol consumption and appears to be a lasting change.
"The epigenetic changes we have observed in the amygdala of early drinkers can alter the normal functioning of the amygdala, which helps regulate our emotions and can make individuals more vulnerable to anxiety." said Pandey.
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