Anorexia nervosa is an eating disorder in which people become obsessive about food intake and weight. Anorexia may begin with regular dieting, but in the disorder, eating is severely limited. Scientists don't know what causes anorexia, although there are some risk factors including family influences, developmental issues, and genetic factors. Sports that are focused on certain body shapes or sizes, such as cheerleading or wrestling, can increase the risk of anorexia as well.
Anorexia has also been linked to anxiety and depression, which has suggested that anorexia may share some biological mechanisms with parts of the brain that are involved in emotional regulation. The amygdala is one area of the brain that is important to the processing of emotions. A new study published in Cell Reports has now suggested that anorexia is caused by the activity of specific subpopulations of neurons in the amygdala.
Certain neurons, which are identifiable by the expression of a molecule called protein kinase C-delta (PKC-delta), have been shown to be related to anorexia. In this work, the researchers showed that these neurons are central to the development of anorexia in an animal model of the disorder.
The researchers determined that as anorexia was developing in the mouse model, the activity of these PKC-delta neurons was also found to increase during eating. If the PKC-delta neurons were artificially stimulated, the mice began eating less and exercising more.
According to the study, the PKC-delta neurons are located in two parts of the amygdala: the central nucleus (CeA) and the oval region of the bed nucleus of the stria terminalis (ovBNST).
When these neurons were lost from the animal model of anorexia, the disorder never developed, but they had to be ablated from both regons of the amygdala to relieve the disease; ablation of only one neuronal subset was not sufficient to stop anorexia from developing.
"This study suggests two important insights to treat anorexia. One is that we need to target multiple brain regions to develop therapies. We also need to treat multiple conditions," said senior study author Haijiang Cai, a University of Arizona associate professor in the Department of Neuroscience and BIO5 Institute member. "For example, maybe one drug will target nausea and another drug target will target inflammation, and you have to combine them, like a cocktail therapy, to have better therapeutic effects."
Of course, in order to do all of this research on neurons in the brain, the scientists had to rely on mouse models, which they acknowledged to not recapitulate the human disease exactly. However, Cai noted that there are several commonalities. These include limited food intake, excessive exercise, and very low body weight. "We can't know if an animal has a warped body image, but we can measure the other three features."
Researchers also won't be able to use the destruction of human neurons as a treatment method. But it may be possible to create methods to tamp down their activity or silence them, which could help people who are already in recovery for the disorder.
Sources: University of Arizona, Cell Reports
