Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2013) 32 P703 | DOI: 10.1530/endoabs.32.P703

ECE2013 Poster Presentations Neuroendocrinology (42 abstracts)

Neurodegenerative and inflammatory biomarkers in cerebrospinal fluid in patients with Cushing's syndrome

Oskar Ragnarsson 1 , Peter Berglund 2 , Detek N Eder 3 , Henrik Zetterberg 2 , Max A Hietala 2 , Kaj Blennow 2 & Gudmundur Johannsson 1


1Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden; 2Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden; 3Vigilance and Neurocognition Laboratory at Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden.


Background: Patients with Cushing’s syndrome (CS) in long-term remission have impaired cognitive function. Cerebrospinal fluid (CSF) biomarkers are important diagnostic tools in the work-up of patients with cognitive impairment. The aim of this study was to analyze biological markers in CSF from patients with CS in remission. Owing to the overlapping similarities between patients with CS and dementia, i.e. cognitive dysfunction and hypercortisolemia, the main hypothesis was that the pattern of CSF biomarkers in CS patients resembles the pattern found in other neurodegenerative disorders.

Patients and methods: This was a cross-sectional, case-controlled, single centre study. Twelve women previously treated for CS, six matched controls (age and educational level) and three women with active CS were studied. The following neurodegenerative CSF markers; total τ, hyperphosphorylated τ, amyloid β peptides (Aβ1–42, Aβ38, Aβ40 and Aβ42), soluble amyloid precursor protein α and β, neurofilament light proteins, glial fibrillary acidic protein and monocyte chemoattractant protein 1, and inflammatory CSF markers; interferon-gamma, interleukin β (ILβ), IL2, IL4, IL5, IL8, IL10, IL12p70, IL13 and tumour necrosis factor α were analysed.

Results: The mean age (mean±S.D.) was similar in patients with CS in remission (44.9±14 years) and controls (42.3±15.7 years; P=0.726). No differences were seen in concentrations of any neurodegenerative biomarkers between either patients with CS in remission and controls or between patients with active CS and controls. Nor was the concentration of inflammatory biomarkers different between the groups, except for IL8 which was significantly higher in patients with active CS compared to controls.

Conclusions: The pattern of neurodegenerative and inflammatory biomarkers in CSF from patients with CS does not differ from healthy controls. The underlying mechanisms of the cognitive deficits in CS are different from those seen in neurodegenerative disorders and remains to be explained.

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