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Levels of islet amyloid polypeptide in cerebrospinal fluid and plasma from patients with Alzheimers disease
Lund Univ, Sweden.
Lund Univ, Sweden.
Lund Univ, Sweden.
Lund Univ, Sweden.
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2019 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 14, no 6, article id e0218561Article in journal (Refereed) Published
Abstract [en]

The biologically active pancreatic hormone peptide islet amyloid polypeptide (IAPP) regulates brain functions such as appetite and cognition. It also plays a role in clearance of amyloid beta (A beta), a peptide implicated in the dementia disorder Alzheimers disease (AD). If IAPP becomes modified, it loses its biological activity and starts to aggregate. Such aggregations have been found in the AD brain and decreased plasma levels of the unmodified IAPP (uIAPP) have been shown in the same patients. In the current study, we analyze levels of uIAPP and total IAPP (unmodified and modified) in cerebrospinal fluid (CSF) to investigate its potential as a biomarker for AD. We found no differences in neither CSF nor plasma levels of uIAPP or total IAPP in AD patients compared to cognitive healthy individuals (NC). The levels of uIAPP in CSF of NC were positively correlated with uIAPP in plasma, Q-albumin and albumin levels in CSF, but negatively correlated with CSF levels of t-tau and p-tau. These findings were not seen in AD patients. Levels of total CSF IAPP correlated positively with total Q-albumin and albumin levels in CSF in both AD and NC. In addition, total plasma IAPP correlated positively with CSF t-tau and p-tau in NC and negatively with CSF A beta(42) in AD patients. To conclude, our studies did not find evidence supporting the use of CSF IAPP as an AD biomarker. However, our findings, indicating a compromised translocation of uIAPP in and out of the brain in AD patients as well as the correlations between total plasma IAPP and AD biomarkers, encourage further research on the role for IAPP in AD.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE , 2019. Vol. 14, no 6, article id e0218561
National Category
Neurology
Identifiers
URN: urn:nbn:se:liu:diva-160629DOI: 10.1371/journal.pone.0218561ISI: 000484890300040PubMedID: 31206565OAI: oai:DiVA.org:liu-160629DiVA, id: diva2:1360199
Note

Funding Agencies|Swedish Research CouncilSwedish Research Council [521-2013-3448]; Petrus and Augusta Hedlund foundation [20160493]; Swedish Dementia foundation; Ake Wiberg foundation [M17-0025]; Ahlen foundation [mC23 h18]; Crafoord foundation [20180776]; Greta and Johan Kocks foundations; Alzheimer foundation [AF-640421]; Olle Engkvist [194-0643]; Olle Engkvist foundation; Segerfalk foundation

Available from: 2019-10-11 Created: 2019-10-11 Last updated: 2019-12-03

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Nägga, Katarina
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Division of Neuro and Inflammation ScienceFaculty of Medicine and Health SciencesDepartment of Acute Internal Medicine and Geriatrics
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