Psychoneuroendocrinology. 2021 Oct 28;135:105576. doi: 10.1016/j.psyneuen.2021.105576. Online ahead of print.
ABSTRACT
PURPOSE: The acute state of anorexia nervosa (AN) is accompanied by increased peripheral concentrations of brain-derived damage markers indicative of ongoing neural and glial damage processes. Although these findings correspond with well-documented structural brain changes in the disorder, it remains unclear whether abnormal levels of brain-derived damage markers persist after long-term weight-recovery from AN.
METHODS: To address this question, we used single-molecule array (Simoa) technology to measure serum levels of neurofilament light (NF-L), tau protein and glial fibrillary acidic protein (GFAP) in a group of 55 long-term weight-recovered women with a history of AN (recAN) and 55 age-matched healthy controls. Strict exclusion criteria allowed us to control for confounds present in previous studies including most importantly neurological conditions.
RESULTS: We found not only no group differences but also statistical evidence for equal damage marker levels between groups using Bayesian hypothesis testing.
CONCLUSION: These results provide evidence for the absence of neuronal and glial damage processes after long-term weight-recovery from AN. Together, our findings are indicative of complete normalization following long-term weight restoration provide hope that recovery from AN halts neuronal damage processes and support the need to test potential candidates for therapeutic interventions including pharmacological neuroprotection.
PMID:34781223 | DOI:10.1016/j.psyneuen.2021.105576
