Different pattern of CSF glial markers between dementia with Lewy bodies and Alzheimer’s disease

Estrella Morenas-Rodríguez, Daniel Alcolea, Marc Suárez-Calvet, Laia Muñoz-Llahuna, Eduard Vilaplana, Isabel Sala, Andrea Subirana, Marta Querol-Vilaseca, María Carmona-Iragui, Ignacio Illán-Gala, Roser Ribosa-Nogué, Rafael Blesa, Christian Haass, Juan Fortea, Alberto Lleó

    Research output: Contribution to journalArticleResearch

    6 Citations (Scopus)

    Abstract

    © 2019, The Author(s). The role of innate immunity in dementia with Lewy bodies (DLB) has been little studied. We investigated the levels in cerebrospinal fluid (CSF) of glial proteins YKL-40, soluble TREM2 (sTREM2) and progranulin in DLB and their relationship with Alzheimer’s disease (AD) biomarkers. We included patients with DLB (n = 37), prodromal DLB (prodDLB, n = 23), AD dementia (n = 50), prodromal AD (prodAD, n = 53), and cognitively normal subjects (CN, n = 44). We measured levels of YKL-40, sTREM2, progranulin, Aβ1–42, total tau (t-tau) and phosphorylated tau (p-tau) in CSF. We stratified the group DLB according to the ratio t-tau/Aβ1–42 (≥0.52, indicative of AD pathology) and the A/T classification. YKL-40, sTREM2 and progranulin levels did not differ between DLB groups and CN. YKL-40 levels were higher in AD and prodAD compared to CN and to DLB and prodDLB. Patients with DLB with a CSF profile suggestive of AD copathology had higher levels of YKL-40, but not sTREM2 or PGRN, than those without. T+ DLB patients had also higher YKL-40 levels than T−. Of these glial markers, only YKL-40 correlated with t-tau and p-tau in DLB and in prodDLB. In contrast, in prodAD, sTREM2 and PGRN also correlated with t-tau and p-tau. In conclusion, sTREM2 and PGRN are not increased in the CSF of DLB patients. YKL-40 is only increased in DLB patients with an AD biomarker profile, suggesting that the increase is driven by AD-related neurodegeneration. These data suggest a differential glial activation between DLB and AD.
    Original languageEnglish
    Article number7803
    JournalScientific Reports
    Volume9
    DOIs
    Publication statusPublished - 1 Dec 2019

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