Increased soluble TREM2 in cerebrospinal fluid is associated with reduced cognitive and clinical decline in Alzheimer’s disease
Open accessAbstract
Higher CSF sTREM2 concentrations are associated with slower rates of cognitive decline in subjects with Alzheimer’s disease.
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Increased sTREM2 inhibits fibrillization of Aβ peptides, increases uptake of Aβ fibrils into microglial cells, and attenuates cognitive and clinical decline in AD patients and AD mouse models.
“Epidemiologic study of AD patients revealed that increased sTREM2 was shown to be beneficial: it can inhibit the fibrillization of Aβ peptides, increase the uptake of Aβ fibrils into microglial cells,235 and attenuate cognitive and clinical decline in AD patients and AD mouse models.236,237”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [236]
The Abstract reports that higher CSF sTREM2 was associated with slower cognitive decline and clinical progression in people with biomarker-confirmed AD. The Discussion cautions that this observational finding does not establish a causal effect. Its mouse-model discussion concerns TREM2 function and pathology, not evidence that increased sTREM2 attenuates cognitive or clinical decline in AD mice; the fibrillization and uptake claims are attached to a different citation in the citing sentence. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPatients carrying R47H exhibit higher levels of total tau and phosphorylated tau in CSF compared to non-carriers.
“patients carrying this mutation exhibit higher levels of both total tau and phosphorylated tau in CSF compared to non-carriers [104]”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [104]
The Discussion reports an association between CSF sTREM2 and higher CSF p-tau181 and total tau, but it does not compare R47H carriers with non-carriers. Searches for R47H and carrier comparisons found no passage addressing the claimed difference. (LLM, conf=0.75)
Experimental — accuracy not yet measuredMicroglial activation may also be protective in neurodegenerative conditions, for example by enhancing microglia phagocytosis of amyloid plaques in the context of AD.
“However, microglial activation may also be protective in these neurodegenerative conditions, for example by enhancing microglia phagocytosis of amyloid plaques in the context of AD (176–178).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [176]
Higher CSF sTREM2/p-Tau is associated with slower cognitive decline.
“higher CSF sTREM2/p-Tau was associated with slower cognitive decline”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [188]
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References 70 · Cited by 327
Research works printed but not linked: 1
- [4]Guerreiro R, Hardy J, TREM2 and neurodegenerative disease. N. Engl. J. Med 369, 1569– 1570 (2013). 24143816
- Authors
- Ewers, M., Franzmeier, N., Suárez-Calvet, M., Morenas-Rodriguez, E., Caballero, M. A. A., Kleinberger, G., Piccio, L., Cruchaga, C., Deming, Y., Dichgans, M., Trojanowski, J. Q., Shaw, L. M., Weiner, M. W., Haass, C., & Initiative, A. D. N.
- Affiliations
- LMU Klinikum (DE)
- Chair of Metabolic Biochemistry, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität München, Munich, Germany.
- Institute for Stroke and Dementia Research, University Hospital Munich, LMU, Munich, Germany.
- Munich Cluster for Systems Neurology (DE)
- The University of Sydney (AU)
- Washington University in St. Louis (US)
- German Center for Neurodegenerative Diseases (DE)
- University of Pennsylvania (US)
- University of California, San Francisco (US)
- Corresponding author
- Ewers, Michael
- Franzmeier, Nicolai
- Haass, Christian
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2019-08-28
- Volume
- 11
- Issue
- 507
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC7050285
- OpenAlex
- W2971202256
- Cited by
- 327
- References
- 70
- Citations by year
- 2026: 40 · 2025: 49 · 2024: 53 · 2023: 40 · 2022: 60 · 2021: 42 · 2020: 38 · 2019: 5
- FWCI
- 15.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Open access LMU (Ludwid Maxmilian's Universitat Munchen) (submittedVersion)
- DZNE Pub (submittedVersion)
- Funders
- National Institutes of Health (R01AG044546, P01AG003991, RF1AG053303, R01AG058501, U01AG058922, U01 AG024904)
- U.S. Department of Defense (W81XWH-12-2-0012)
- Deutsche Forschungsgemeinschaft (EXC 1010 SyNergy, HA1737/16-1)
- Cure Alzheimer’s Fund
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- soluble TREM2, TREM2, Alzheimer's disease, cerebrospinal fluid biomarkers, cognitive decline, clinical deterioration, innate immune response, neuroinflammation
- MeSH terms
- Alzheimer Disease, Cognition, Cross-Sectional Studies, Humans, Membrane Glycoproteins, Neuropsychological Tests, Receptors, Immunologic, Amyloid beta-Peptides, tau Proteins
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