A high cerebrospinal fluid soluble TREM2 level is associated with slow clinical progression of Alzheimer's disease.
Alzheimer's disease
Clinical Dementia Rating scale
disease progression
soluble triggering receptor expressed on myeloid cells 2 (sTREM2)
trajectories
Journal
Alzheimer's & dementia (Amsterdam, Netherlands)
ISSN: 2352-8729
Titre abrégé: Alzheimers Dement (Amst)
Pays: United States
ID NLM: 101654604
Informations de publication
Date de publication:
2020
2020
Historique:
received:
05
08
2020
revised:
08
10
2020
accepted:
08
10
2020
entrez:
14
12
2020
pubmed:
15
12
2020
medline:
15
12
2020
Statut:
epublish
Résumé
The progression rate of Alzheimer's disease (AD) varies and might be affected by the triggering receptor expressed on myeloid cells (TREM2) activity. We explored if cerebrospinal fluid (CSF) soluble TREM2 (sTREM2), a proxy of microglial activity, is associated with clinical progression rate. Patients with clinical AD (N = 231) were followed for up to 3 years after diagnosis. Cognitively healthy controls (N = 42) were followed for 5 years. CSF sTREM2 was analyzed by enzyme-linked immunosorbent assay. Group-based trajectory modeling revealed distinct clinical progression groups. Higher CSF sTREM2 was associated with slow clinical progression. The slow- and medium-progressing groups had higher CSF sTREM2 than the cognitively healthy, who had a similar level to patients with rapid clinical progression. CSF sTREM2 levels were associated with clinical progression in AD, regardless of core biomarkers. This could be useful in assessing disease development in relation to patient care and clinical trial recruitment.
Identifiants
pubmed: 33313376
doi: 10.1002/dad2.12128
pii: DAD212128
pmc: PMC7720866
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e12128Informations de copyright
© 2020 The Authors. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals, LLC on behalf of Alzheimer's Association.
Déclaration de conflit d'intérêts
Dr. Edwin, Dr. Persson, and Dr. Knapskog report work with Roche BN29553; Dr. Edwin, Dr. Knapskog, and Dr. Saltvedt report work with Boehringer‐Ingelheim 1346.0023, outside the submitted work. Dr. Nilsson has received an honorarium from BioArctic, and has a collaboration with this company, outside the submitted work. The other authors declare no conflicts of interest.
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