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Early increase of CSF sTREM2 in Alzheimer's disease is associated with tau related-neurodegeneration but not with amyloid-β pathology.

著者 Suárez-Calvet M , Morenas-Rodríguez E , Kleinberger G , Schlepckow K , Caballero MÁA , Franzmeier N , Capell A , Fellerer K , Nuscher B , Eren E , Levin J , Deming Y , Piccio L , Karch CM , Cruchaga C , Shaw LM , Trojanowski JQ , Weiner M , Ewers M , Haas
Mol Neurodegener.2019 Jan 10 ; 14(1):1.
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TREM2 is a transmembrane receptor that is predominantly expressed by microglia in the central nervous system. Rare variants in the TREM2 gene increase the risk for late-onset Alzheimer's disease (AD). Soluble TREM2 (sTREM2) resulting from shedding of the TREM2 ectodomain can be detected in the cerebrospinal fluid (CSF) and is a surrogate measure of TREM2-mediated microglia function. CSF sTREM2 has been previously reported to increase at different clinical stages of AD, however, alterations in relation to Amyloid β-peptide (Aβ) deposition or additional pathological processes in the amyloid cascade (such as tau pathology or neurodegeneration) remain unclear. In the current cross-sectional study, we employed the biomarker-based classification framework recently proposed by the NIA-AA consensus guidelines, in combination with clinical staging, in order to examine the CSF sTREM2 alterations at early asymptomatic and symptomatic stages of AD.
PMID: 30630532 [PubMed - in process]
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