Research has investigated the relationship between impulsivity, alcohol dependence, and P3 amplitude, which is an electrical brain response. In a study using a visual oddball task, alcohol-dependent individuals showed lower P3 amplitudes and reduced activation in frontal brain regions. They also had higher impulsivity scores, which were negatively correlated with P3 amplitude. These findings highlight the frontal focus of reduced activation in alcohol-dependent individuals and those with higher impulsivity

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There are three components that research has reported to be relevant to understand biological extensions of AUDs: 

- Genetic Mechanisms
- Neuroanatomical Substrates
- Electrophysiological Data

Biological extensions of AUDs

Lejuez, C.W., et al. “Behavioral and Biological Indicators of Impulsivity in the Development of Alcohol Use, Problems, and Disorders.” Alcoholism: Clinical and Experimental Research, 2010, https://doi.org/10.1111/j.1530-0277.2010.01217.x. 

Behavioral and Biological Indicators of Impulsivity in the Development of Alcohol Use, Problems, and Disorders

Genetic factors play a significant role in the traits associated with alcohol use disorders (AUDs). Several studies have explored the genetic basis of impulsivity, a characteristic linked to AUDs. For instance, variations in the 5-HT2A receptor gene and the dopamine receptor D2 (DRD2) gene have been associated with impulsivity in alcohol-dependent individuals. Additionally, the tryptophan hydroxylase (TPH) gene, which is involved in serotonin biosynthesis, has been implicated in alcoholism and impulsivity. Although the specific relationships between these genes and impulsivity are not fully understood, these findings suggest a connection between serotonin function and alcoholism. Understanding the genetic pathways involved in impulsivity can contribute to our understanding of the neurochemical mechanisms underlying the development of alcohol abuse.

Genetic Mechanisms of AUDs

Alcohol-dependent individuals exhibit altered neural responses related to reward and impulsivity. They show reduced activation in the ventral striatum during non-alcohol-related reward tasks but increased activation when exposed to alcohol cues. Impaired activation is also observed in brain regions involved in behavioral control, such as the dorsolateral prefrontal cortex, during tasks assessing response inhibition and risk-taking. Individual differences in neural activation are related to externalizing symptoms, psychopathology, and affect. These findings suggest shared vulnerabilities between disruptive/antisocial behavior disorders and alcohol use disorders, indicating common dysfunction across related conditions.

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