Abstract

Atrophic brain changes in acute anorexia nervosa (AN) are often visible to the naked eye on computed tomography or magnetic resonance imaging scans, but it remains unclear what is driving these effects. In neurological diseases, neurofilament light (NF-L) and tau protein have been linked to axonal damage. Glial fibrillary acidic protein (GFAP) has been associated with astroglial injury. In an attempt to shed new light on factors potentially underlying past findings of structural brain alterations in AN, the current study investigated serum NF-L, tau protein, and GFAP levels longitudinally in AN patients undergoing weight restoration. Blood samples were obtained from 54 acutely underweight, predominantly adolescent female AN patients and 54 age-matched healthy control participants. AN patients were studied in the severely underweight state and again after short-term partial weight restoration. Group comparisons revealed higher levels of NF-L, tau protein, and GFAP in acutely underweight patients with AN compared to healthy control participants. Longitudinally, a decrease in NF-L and GFAP but not in tau protein levels was observed in AN patients upon short-term partial weight restoration. These results may be indicative of ongoing neuronal and astroglial injury during the underweight phase of AN. Normalization of NF-L and GFAP but not tau protein levels may indicate an only partial restoration of neuronal and astroglial integrity upon weight gain after initial AN-associated cell damage processes.

Highlights

  • Anorexia nervosa (AN) is a severe eating disorder usually beginning in adolescence characterized by a persistent restriction in energy intake[1] leading to serious medical complications[2,3].It has been known for decades that the brains of patients in the acutely underweight state of AN show signs compatible with atrophic changes[4]

  • Between timepoint one and timepoint two, AN participants showed a significant increase in BMI standard deviation scores (BMI-SDS), a significant decrease in Beck Depression Inventory-II (BDI-II) scores, and a trend towards a decrease in Eating Disorder Inventory-2 (EDI-2) core scores

  • We found elevated levels of neurofilament light (NF-L), tau protein, and Glial fibrillary acidic protein (GFAP)

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Summary

Introduction

It has been known for decades that the brains of patients in the acutely underweight state of AN show signs compatible with atrophic changes[4]. Magnetic resonance imaging (MRI) studies have found alterations in brain structure such as substantial reductions in white and gray. The investigation of brain-derived proteins may aid our understanding of the underlying biology of dynamic brain changes in AN. Such proteins can be measured in cerebrospinal fluid (CSF) or in blood samples and are often associated with specific processes on cellular level[9,10]. Measurements in blood have in the past been limited by the relatively lower

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