Vis enkel innførsel

dc.contributor.authorNordengen, Kaja
dc.contributor.authorKirsebom, Bjørn-Eivind
dc.contributor.authorHenjum, Kristi
dc.contributor.authorSelnes, Per
dc.contributor.authorGisladottir, Berglind
dc.contributor.authorWettergreen, Marianne
dc.contributor.authorTorsetnes, Silje Bøen
dc.contributor.authorGrøntvedt, Gøril Rolfseng
dc.contributor.authorWaterloo, Knut
dc.contributor.authorAarsland, Dag
dc.contributor.authorNilsson, Lars
dc.contributor.authorFladby, Tormod
dc.description.abstractBackground Neuronal and glial cell interaction is essential for synaptic homeostasis and may be affected in Alzheimer’s disease (AD). We measured cerebrospinal fluid (CSF) neuronal and glia markers along the AD continuum, to reveal putative protective or harmful stage-dependent patterns of activation. Methods We included healthy controls (n = 36) and Aβ-positive (Aβ+) cases (as defined by pathological CSF amyloid beta 1-42 (Aβ42)) with either subjective cognitive decline (SCD, n = 19), mild cognitive impairment (MCI, n = 39), or AD dementia (n = 27). The following CSF markers were measured: a microglial activation marker—soluble triggering receptor expressed on myeloid cells 2 (sTREM2), a marker of microglial inflammatory reaction—monocyte chemoattractant protein-1 (MCP-1), two astroglial activation markers—chitinase-3-like protein 1 (YKL-40) and clusterin, a neuron-microglia communication marker—fractalkine, and the CSF AD biomarkers (Aβ42, phosphorylated tau (P-tau), total tau (T-tau)). Using ANOVA with planned comparisons, or Kruskal-Wallis tests with Dunn’s pairwise comparisons, CSF levels were compared between clinical groups and between stages of biomarker severity using CSF biomarkers for classification based on amyloid pathology (A), tau pathology (T), and neurodegeneration (N) giving rise to the A/T/N score. Results Compared to healthy controls, sTREM2 was increased in SCD (p < .01), MCI (p < .05), and AD dementia cases (p < .001) and increased in AD dementia compared to MCI cases (p < .05). MCP-1 was increased in MCI (p < .05) and AD dementia compared to both healthy controls (p < .001) and SCD cases (p < .01). YKL-40 was increased in dementia compared to healthy controls (p < .01) and MCI (p < .05). All of the CSF activation markers were increased in subjects with pathological CSF T-tau (A+T−N+ and A+T+N+), compared to subjects without neurodegeneration (A−T−N− and A+T−N−). Discussion Microglial activation as indicated by increased sTREM2 is present already at the preclinical SCD stage; increased MCP-1 and astroglial activation markers (YKL-40 and clusterin) were noted only at the MCI and AD dementia stages, respectively, and in Aβ+ cases (A+) with pathological T-tau (N+). Possible different effects of early and later glial activation need to be explored.nb_NO
dc.publisherBMC (part of Springer Nature)nb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleGlial activation and inflammation along the Alzheimer's disease continuumnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalJournal of Neuroinflammationnb_NO
dc.description.localcode© The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (
cristin.unitnameInstitutt for nevromedisin og bevegelsesvitenskap

Tilhørende fil(er)


Denne innførselen finnes i følgende samling(er)

Vis enkel innførsel

Navngivelse 4.0 Internasjonal
Med mindre annet er angitt, så er denne innførselen lisensiert som Navngivelse 4.0 Internasjonal