Binge drinking during teenage life has been shown to lasting impact on the brain wirings and is linked to higher risk of alcohol use disorder and psychological problems later in life.
In a recent study, a team of researchers at the Center for Alcohol Research in Epigenetics (CARE) at the University of Illinois, Chicago has demonstrated that these lasting effects are due to epigenetic changes that alter the expression of a protein important for the formation and upkeep of neural networks in the amygdala, an area of the brain responsible for fear, anxiety, and emotion.
Findings of the study are based on assessment of postmortem human brain tissue, detailed in a paper appeared in the journal Translational Psychiatry.
The team studied the postmortem human amygdala tissue samples taken from the brains of total 44 individuals – 11 early-onset drinkers or who began drinking seriously before the age of 21; 11 late-onset drinkers or who began drinking heavily after the age of 21; and 22 people with no history of any alcohol use disorder. The average age of death of these individuals was 55 years old for the early-onset drinkers, 59 for late-onset drinkers, and 58 for those with no alcohol use disorder.
According to the researchers, amygdalae of individuals identified as early-onset drinker had around 30% more of a molecule known as BDNF-AS, a large non-coding RNA. It is a type of RNA which is not involved in the production of protein from DNA, instead, it regulates a gene responsible for producing a protein called BDNF. This protein serves as a growth factor and is essential for the normal formation and maintenance of synapses of the brain. The amount of BDNF-AS is indirectly proportional to the amount of BDNF.
The team found that BDNF is 30%-40% lesser in the brain tissue of individuals who began drinking before the age of 21 than in the brain tissue of individuals without alcohol use disorder. This BDNF reduction was not seen in the brain tissue of both late-onset drinkers and individuals with no history of alcohol use disorder.
Corresponding author Subhash Pandey said that the epigenetic changes to the molecule BDNF-AS may be the reason why BDNF is reduced in the amygdalae from individuals who began consuming alcohol early in life. No changes were seen in the amygdalae from individuals who began drinking after the age of 21, he added.
BDNF is necessary for the normal brain development as well as the formation of neuron connections, according to Pandey, if levels are reduced because of alcohol exposure, the brain is unlikely to develop normally.
The team also discovered that the high BDNF-AS in the early-onset drinkers is due to lowered methylation of BDNF-AS, which is believed to be caused by starting to drink heavily early in life, leading to a long-lasting change.
Such epigenetic changes in the amygdala of early-onset drinkers could further alter the normal function of amygdala or the development and maintenance of alcohol use disorder later in life, the researchers said.