Neurogranin and YKL-40: independent markers of synaptic degeneration and neuroinflammation in Alzheimer's disease. Issue 1 (December 2015)

• Record Type: Journal Article
• Authors: Hellwig, Konstantin; Kvartsberg, Hlin; Portelius, Erik; Andreasson, Ulf; Oberstein, Timo; Lewczuk, Piotr; Blennow, Kaj; Kornhuber, Johannes; Maler, Juan; Zetterberg, Henrik; Spitzer, Philipp
• Is Part Of: Alzheimer's research & therapy. Volume 7:Issue 1(2015)
• Page Start: 1
• Page End: 8
• Publication Date: 2015-12
• Subjects: Alzheimer's disease -- Periodicals; 616.831005
• DOI: 10.1186/s13195-015-0161-y
• Languages: English
• ISSNs: 1758-9193

Abstract

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 andp < 0.05 for MCI-AD) and YKL-40 (p < 0.05 for AD-D andp = 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.