Stress-Induced Brain Damage Could Possibly Be Prevented With An Experimental Drug
Nearly 75 percent of Americans report experiencing at least one symptom of stress in the past month, including irritability, anxiety, fatigue, and depression, according to a 2015 survey from the American Psychological Association (APA). According to previous studies, stress has been shown to cause alterations to the hippocampus – the part of the brain responsible for memory and emotion – which can trigger anxiety and depression.
Very few studies have investigated how stress affects the amygdala – a brain region involved in fear and anxiety, noted by the team in research notes. Stress impairs nerve cell communication in amygdala’s medial region.
“Chronic stress is linked to a number of psychiatric conditions, and this research may offer some new insights on their pathology.” noted Bruce S. McEwen.
In a recent study published in the journal Molecular Psychiatry, a team of researchers at Rockefeller University in New York has shed some light on the structural brain changes as stress leads to anxiety and depression. Led by Carla Nasca and colleagues, the study aim was to find ways treat and prevent both anxiety and depression.
In order to induce prolonged stress in mice, researchers periodically confined the rodents to a small space for 21 days. At the end of the confinement period, the behavior of the mice was analyzed by the team. Specifically, they looked at whether the mice started to display behaviors related to anxiety and depression – such as social interaction avoidance.
Researchers also assessed the rodents’ neurons (nerve cells), in specific areas of the amygdala, including the medial and basolateral regions. Performing well were neuronal branches in the basolateral region progressively lengthened and became more complex in response to prolonged stress. Nerve cells in the medial region – which are important for communication between other areas of the brain – were found to shrink in size in response to prolonged stress.
According to the researchers, this is the side effect of stress that can be damaging to the brain, even triggering anxiety and depression, by reducing the brain’s ability to accommodate new experiences.
“It seems possible that the contrasting responses we see within the amygdala, and the limbic system in general, may contribute to these disorders’ differing symptoms, which can range from avoiding social contact to experiencing vivid flashbacks.” added Bruce S. McEwen, study co-author
On a brighter note, the researchers also found that Acetyl-l-carnitine prevented neuronal branch shrinkage, which led to another 21-day stress-inducing experiment round in another group of mice.
This time, mice were treated with acetyl-l-carnitine 3 days before the end of the experiment – a molecule naturally produced by both humans and mice. Studies have shown that animals susceptible to depression are more likely to be deficient in acetyl-l-carnitine, and it is currently being tested as an antidepressant.
Mice that received acetyl-l-carnitine demonstrated greater neuronal branching in the medial region of the amygdala and were found to be were more sociable at the end of the experiment, compared with the untreated mice. Based on the results, the researchers suggest acetyl-l-carnitine might have the ability to prevent some harmful brain changes that occur in response to stress.
Next, the team plans to investigate whether humans with depression have lower levels of acetyl-l-carnitine than those without the condition.