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Alzheimers Res Ther. 2015 Dec 24;7:74. doi: 10.1186/s13195-015-0161-y.

Neurogranin and YKL-40: independent markers of synaptic degeneration and neuroinflammation in Alzheimer's disease.

Author information

1
Department of Psychiatry and Psychotherapy, University clinic Erlangen and Friedrich-Alexander University Erlangen-Nürnberg, Schwabachanlage 6, 91054, Erlangen, Germany. konstantin.hellwig@uk-erlangen.de.
2
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. hlin.johansson-schmidt@neuro.gu.se.
3
AlzeCure Foundation, Karolinska Institutet Science Park, Huddinge, Sweden. hlin.johansson-schmidt@neuro.gu.se.
4
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. erik.portelius@neuro.gu.se.
5
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. ulf.andreasson@neuro.gu.se.
6
Department of Psychiatry and Psychotherapy, University clinic Erlangen and Friedrich-Alexander University Erlangen-Nürnberg, Schwabachanlage 6, 91054, Erlangen, Germany. timo.oberstein@uk-erlangen.de.
7
Department of Psychiatry and Psychotherapy, University clinic Erlangen and Friedrich-Alexander University Erlangen-Nürnberg, Schwabachanlage 6, 91054, Erlangen, Germany. piotr.lewczuk@uk-erlangen.de.
8
Department of Neurodegeneration Diagnostics, Medical University of Białystok, Białystok, Poland. piotr.lewczuk@uk-erlangen.de.
9
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. kaj.blennow@neuro.gu.se.
10
Department of Psychiatry and Psychotherapy, University clinic Erlangen and Friedrich-Alexander University Erlangen-Nürnberg, Schwabachanlage 6, 91054, Erlangen, Germany. johannes.kornhuber@uk-erlangen.de.
11
Department of Psychiatry and Psychotherapy, University clinic Erlangen and Friedrich-Alexander University Erlangen-Nürnberg, Schwabachanlage 6, 91054, Erlangen, Germany. manuel.maler@uk-erlangen.de.
12
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. henrik.zetterberg@clinchem.gu.se.
13
Department of Molecular Neuroscience, UCL Institute of Neurology, London, WC1N 3BG, UK. henrik.zetterberg@clinchem.gu.se.
14
Department of Psychiatry and Psychotherapy, University clinic Erlangen and Friedrich-Alexander University Erlangen-Nürnberg, Schwabachanlage 6, 91054, Erlangen, Germany. philipp.spitzer@uk-erlangen.de.

Abstract

INTRODUCTION:

Neuroinflammation and synaptic degeneration are major neuropathological hallmarks in Alzheimer's disease (AD). Neurogranin and YKL-40 in cerebrospinal fluid (CSF) are newly discovered markers indicating synaptic damage and microglial activation, respectively.

METHODS:

CSF samples from 95 individuals including 39 patients with AD dementia (AD-D), 13 with mild cognitive impairment (MCI) due to AD (MCI-AD), 29 with MCI not due to AD (MCI-o) and 14 patients with non-AD dementias (non-AD-D) were analyzed for neurogranin and YKL-40.

RESULTS:

Patients with dementia or MCI due to AD showed elevated levels of CSF neurogranin (p < 0.001 for AD-D and p < 0.05 for MCI-AD) and YKL-40 (p < 0.05 for AD-D and p = 0.15 for MCI-AD) compared to mildly cognitively impaired subjects not diagnosed with AD. CSF levels of neurogranin and YKL-40 did not differ between MCI not due to AD and non-AD dementias. In AD subjects no correlation between YKL-40 and neurogranin was found. The CSF neurogranin levels correlated moderately with tau and p-tau but not with Aβ42 or the MMSE in AD samples. No relevant associations between YKL-40 and MMSE or the core AD biomarkers, Aβ42, t-tau and p-tau were found in AD subjects.

CONCLUSIONS:

Neurogranin and YKL-40 are promising AD biomarkers, independent of and complementary to the established core AD biomarkers, reflecting additional pathological changes in the course of AD.

PMID:
26698298
PMCID:
PMC4690296
DOI:
10.1186/s13195-015-0161-y
[Indexed for MEDLINE]
Free PMC Article

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