The Genetic Basis of Traumatic Memories

A new paper in Nature Neuroscience reveals the genetic basis for the ability to recall emotionally charged events. The gene in question is ADRA2B, which codes for the α2b-adranergic receptor. Quervain et al. found that Swiss subjects were better at recalling arousing images if they possessed a version of the receptor that lacked three amino acids. While the deletion variant significantly enhanced memories of emotional images, it did not effect arousal during the learning phase or memory of neutral images.

Additionally, Quervain et al. genotyped a cohort of Rwandan refugees. They found that subjects possessing the deletion variant were more likely to recall traumatic experiences than those with the full-length ADRA2B gene. It’s rare for scientists to go out of their way to demonstrate the real-world significance of their findings, so this approach should be applauded.

It’s tempting to speculate that the ADRA2B deletion variant could cause Post-Traumatic Stress Disorder (PTSD). However, the authors found no significant correlation between this diagnosis and subjects’ genotypes. More research is needed to clarify the connection, should it exist.

The findings are interesting in light of previous research into adrenergic signalling pathways. Propranolol, a drug that blocks beta-adregnergic receptors, has been shown to impair memory of emotionally charged events. Incidentally, the drug is also used to treat hypertension and essential tremor.

Research into the modulation of traumatic memories raises ethical questions. For instance, should the Army medicate soldiers with propranolol before they enter combat situations so they won’t suffer mental anguish later in life? While this could improve quality of life for veterans, traumatic stories play a crucial role in informing the public about the dangers of war. Though painful, such memories temper our violent and often self-destructive impulses.

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