Journal
CLINICAL MASS SPECTROMETRY
Volume 14, Issue -, Pages 124-129Publisher
ELSEVIER
DOI: 10.1016/j.clinms.2018.10.001
Keywords
Alzheimer's disease; Parathyroid hormone-related protein; PTHrP; Mass spectrometry; Tau protein; Phosphorylated tau protein; Beta-amyloid
Categories
Funding
- Swedish Research Council VR [2014-6447, 2017-00915]
- Royal Society of Arts and Sciences in Gothenburg (KVVS)
- Alzheimerfonden
- Hjarnfonden
- Demensfonden
- Jeanssons Stiftelsen
- Ahlen Stiftelsen
- Ake Wiberg Stiftelsen
- Stiftelsen Gamla Tjanarinnor
- Stohnes Stiftelse
- Torsten Soderberg Foundation
- Stiftelsen Wilhelm och Martina Lundgrens Vetenskapsfond
- Swedish Research Council [2017-00915] Funding Source: Swedish Research Council
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Background: Parathyroid hormone-related protein (PTHrP) is involved in intracellular calcium regulation, neural cell proliferation and synaptic transmission. To date, no studies have been performed to evaluate the potential of PTHrP concentrations in cerebrospinal fluid (CSF) as a biomarker of brain pathophysiology. In this study we evaluated the association between CSF concentrations of PTHrP with the core CSF biomarkers of Alzheimer's disease (AD). Methods: PTHrP and calcium were analysed using validated mass spectrometry based methods in a set of CSF samples that tested positive (n=45) and negative (n=45) for the AD biomarkers, including total tau protein (T-tau), phosphorylated tau protein (P-tau) and amyloid-beta 42 (A beta 42). The measured CSF concentrations of PTHrP and calcium (Ca) were evaluated for association with AD CSF biomarkers. Results: PTHrP and Ca concentrations in CSF samples ranged between 25 and 137 pmol/L and 0.92-1.53 mmol/L, respectively. Higher concentrations of PTHrP were observed in association with increased concentrations of T-tau and P-tau in the AD and the control group; while a stronger correlation was observed in the control group (rho=0.6, p < 0.0001; and rho=0.72, p < 0.0001, for T-tau and P-tau, respectively). Negative correlation was observed between concentrations of PTHrP and A beta 42 in the AD group (rho=0.27, p=0.015). A statistically significantly lower ratio A beta 42/PTHrP was observed in the AD group (p < 0.0001). Conclusion: In the current study, we observed an association of PTHrP concentrations with concentrations of clinically used CSF biomarkers of AD. Concentrations of PTHrP were positively correlated with concentrations of T-tau and P-tau, suggesting an association with neuronal secretion and function, which is reduced upon progression to AD pathology. Our data suggest potential utility of the A beta 42/PTHrP ratio in assessment of AD progression.
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