Glial and neuronal damage markers in patients with anorexia nervosa

Abstract

Anorexia nervosa (AN) commonly arises during adolescence leading to interruptions of somatic and psychological development as well as to atrophic brain changes. It remains unclear whether these brain changes are related to the loss of neurons, glia, neuropil or merely due to fluid shifts. We determined leptin levels and two brain-derived damage markers: glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE) of 43 acute AN patients and 50 healthy control woman (HCW). Peripheral GFAP and NSE concentrations of AN patients were not elevated and not different from HCW. Subjects with particularly low leptin concentration, indicating severe malnutrition, did not show abnormal values either. During weight recovery the marker proteins remained unchanged. Our preliminary results are in line with neuroimaging studies supporting the reversibility of brain changes in AN and do not substantiate hypotheses relying on the extensive damage of brain cells as an explanation for cerebral atrophy in AN.

Global Cortical Thinning in Acute Anorexia Nervosa Normalizes Following Long-Term Weight Restoration

“…The topographically unspecific nature of cortical thinning and subcortical volume "loss" in acAN and seemingly rapid normalization in recAN are suggestive of pseudoatrophy -that is, no actual apoptotic neurodegeneration. This interpretation is supported by previous findings of normal levels of neural and glial damage markers in AN (72). One possibility worthy of future investigation is that reduced CT in acAN may reflect changes in the lipid structure of the neuronal cell wall and myelin resulting from diminished fat consumption (73).…”

Weight Trajectory over 20 Years and Likelihood of Mild Cognitive Impairment or Dementia Among Older Women

“…Atrophy of the mesial temporal cortex, which is involved in feeding behavior and memory, is preferentially involved in AD . Weight loss with aging could potentially accelerate brain atrophy, as occurs during anorexia nervosa in younger adults . As the deficits seen with anorexia nervosa may not fully reverse after weight recovery and leptin's effects on the brain could be cumulative, weight variability with its repeated episodes of weight loss could negatively affect the brain.…”

Brain volume reduction predicts weight development in adolescent patients with anorexia nervosa

“…As there is significant volume recovery upon weight rehabilitation and no increase in apoptotic markers (Ehrlich et al, 2008;Mainz et al, 2012), neuronal cell death is unlikely, as are colloidal/osmotic water shifts that would be expected to rather increase brain volume than be responsible for shrinkage. More likely, human post-mortem studies (Neum€ arker et al, 1997;BenitezBribiesca et al, 1999) and animal studies (Leuba and Rabinowicz, 1979;Garcia-Ruiz et al, 1993) point to reduced neuronal and glial cell sizes as well as fewer dendrites and synapses in GM.…”