What Does the MAOA Gene Do?

Medically Reviewed on 1/12/2023
MAOA Gene
The presence of an abnormal MAOA gene results in monoamine oxidase deficiency.

The MAOA gene predicts aggression and influences the brain’s neural response to psychosocial stress. Also called the “warrior gene,” the MAOA gene provides instructions for making monoamine oxidase A enzyme.

  • Monoamine oxidase A breaks down neurotransmitters such as serotonin, epinephrine, and dopamine.
  • Serotonin helps regulate mood, sleep, emotion, and hunger, whereas epinephrine and norepinephrine control the body's response to stress.
  • Dopamine transmits information within the brain that helps in smooth physical movements. 

Moreover, monoamine oxidase enzyme A helps in the normal development of the baby's brain before birth.

What happens when the MAOA gene does not function properly?

The MAOA gene plays a vital role in making an enzyme called monoamine oxidase A enzyme, which is involved in the breakdown of neurotransmitters such as noradrenalin, serotonin, and dopamine. Improper MAOA gene function may result in the body's neurotransmitters not breaking down.

  • If adrenalin is not broken down, it accumulates, causing an overreaction to external stimuli and hypersensitivity in the fight or flight response.
  • If dopamine is not metabolized, it gets deposited in excess amounts, causing aggressive behavior.
  • Serotonin helps in calming down behavior and low levels of serotonin result in aggressive behavior.

Any impairment in the MAOA gene also results in disturbed rapid eye movement sleep.

In depressive disorders, the increase in the MAOA gene and the decline in serotonin and norepinephrine levels are the major pathogenic factors. The functional polymorphism of the MAOA gene in serotonin is linked to depression. Inhibitors of the MAOA gene are used as first-generation antidepressants.

Which part of the brain is affected by the MAOA gene?

The MAOA gene affects the brain’s specific areas, such as:

  • Amygdala
  • Hippocampus
  • Anterior cingulate cortex
  • Orbitofrontal cortex

SLIDESHOW

17 Everyday Ways to Ease Depression See Slideshow

What causes monoamine oxidase deficiency?

The presence of an abnormal MAOA gene results in monoamine oxidase deficiency. It is a rare condition that results in behavioral and intellectual disabilities that include aggressive, antisocial, and violent behaviors, sometimes also resulting in autistic features.

Some individuals may also experience the following symptoms:

  • Night tremors
  • Sweating
  • Headache
  • Diarrhea
  • Skin flushing
  • Tremors
  • Abnormal hand movements
  • Body twitches
  • Impaired ability of an individual to control behavioral impulses

The signs and symptoms of monoamine oxidase deficiency develop during childhood and are more common in men than women. 

Monoamine oxidase deficiency is caused by mutations in the MAOA gene and is inherited in an X-linked recessive manner.

Can the MAOA gene predict behavioral aggression after provocation?

Evidence from clinical and preclinical studies suggests a link between monoamine oxidase A levels in the brain and aggression. There is limited evidence of the main effect of genotype and some evidence for a gene-by-environment interaction, such that MAOA is less associated with the occurrence of aggressive behavior in a low provocation condition but significantly predicts such behavior in a high provocation situation.

What are the syndromes associated with MAOA gene dysfunction?

Burners syndrome is a rare genetic disorder associated with the MAOA gene dysfunction. This syndrome is associated with low IQ, problematic impulsive behavior, sleep disorders, and mood swings.

Medically Reviewed on 1/12/2023
References
Image Source: iStock image

https://medlineplus.gov/genetics/gene/maoa/#:~:text=The%20MAOA%20gene%20provides%20instructions,chemical%20reaction%20known%20as%20oxidation.

https://rarediseases.info.nih.gov/diseases/3531/monoamine-oxidase-a-deficiency

https://www.pnas.org/doi/10.1073/pnas.0808376106

https://www.frontiersin.org/articles/10.3389/fnbeh.2020.00065/full