CD33 modulates TREM2: convergence of Alzheimer loci
Open accessAbstract
We used a protein quantitative trait analysis in monocytes from 226 individuals to evaluate cross-talk between Alzheimer loci. The NME8 locus influenced PTK2B and the CD33 risk allele led to greater TREM2 expression. There was also a decreased TREM1/TREM2 ratio with a TREM1 risk allele, decreased TREM2 expression with CD33 suppression and elevated cortical TREM2 mRNA expression with amyloid pathology.
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The findings strengthen the growing evidence linking AD to a network of genes expressed in microglia.
“These results reinforce the emerging genetic and epigenetic association between AD and a network of microglial expressed genes2,5,17–21”
From A common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease (2017) · cites this paper as [20]
The paper’s introductory passage (page unavailable) links AD susceptibility variants to innate immune genes and identifies an AD-associated microglial transcriptomic network. Its own results examine interactions among AD loci chiefly in monocytes, supporting the broader link in the claim. The cited paper does not report an epigenetic association, which is also asserted in the verbatim citing sentence. (LLM, conf=0.82)
Experimental — accuracy not yet measuredHuman AD risk gene variants linked to monocytes include TREM2 and CD33; CD33 is linked to diminished Aβ internalization by peripheral monocytes.
“Several human AD risk gene variants have been linked to monocytes, including those related with TREM2 and CD33 [34, 52], the latter of which is linked to diminished Aβ internalization by peripheral monocytes [34].”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [52]
The paper’s indexed text (section labeled Abstract; no page supplied) identifies TREM2 and CD33 as AD susceptibility loci and reports effects of a CD33 risk allele in human monocytes. Its CD33 suppression results concern TREM2 surface expression, not Aβ internalization; searches for Aβ uptake or internalization in peripheral monocytes found no supporting passage. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTrem2+ monocytes can be detected in blood samples.
“As Trem2+ monocytes can be detected in blood samples,77”
From Cystatin C is glucocorticoid responsive, directs recruitment of Trem2+ macrophages, and predicts failure of cancer immunotherapy (2023) · cites this paper as [77]
Genes expressed in myeloid cells display abnormal patterns of chromatin modification in AD mouse models and human samples.
“At the epigenetic level, genes expressed in myeloid cells display abnormal patterns of chromatin modification in AD mouse models and human samples18–20.”
From A common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease (2017) · cites this paper as [20]
The Abstract reports protein-expression and genetic-association findings in human monocytes, not abnormal chromatin modification in myeloid-cell genes. Searches for chromatin modification and histone changes in AD mouse models and human samples found no passage addressing the claim in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredCases received a diagnosis of dementia of the Alzheimer's type based on NINCDS-ADRDA criteria.
“Cases were diagnosed with dementia of the Alzheimer’s type (DAT) according to the NINCDS-ADRDA20.”
From A common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease (2017) · cites this paper as [20]
The Online Methods describe ROS/MAP participants as cognitively normal at enrollment and receiving annual clinical evaluations, but do not state how Alzheimer’s dementia cases were diagnosed. Searches for NINCDS-ADRDA and dementia diagnosis found no passage specifying those criteria; the passages provide no page numbers. (LLM, conf=0.72)
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- Authors
- Chan, G., White, C. C., Winn, P. A., Cimpean, M., Replogle, J. M., Glick, L. R., Cuerdon, N. E., Ryan, K. J., Johnson, K. A., Schneider, J. A., Bennett, D. A., Chibnik, L. B., Sperling, R. A., Bradshaw, E. M., & De Jager, P. L.
- Affiliations
- Broad Institute (US)
- Brigham and Women's Hospital (US)
- Rush University Medical Center (US)
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2015-09-28
- Volume
- 18
- Issue
- 11
- Pages
- 1556-1558
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC4682915
- OpenAlex
- W1851356616
- Cited by
- 162
- References
- 27
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 17 · 2023: 7 · 2022: 13 · 2021: 18 · 2020: 10 · 2019: 17 · 2018: 20 · 2017: 22 · 2016: 18 · 2015: 2
- FWCI
- 15.22
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institute on Aging (R01AG017917, P30-AG 10161, K25AG041906, R01‐AG17917, R01 AG15819, R01AG036836, R01AG048015, U01AG046152, R01AG043617, R01AG015819, P30AG010161, P50AG005134, RF1AG015819, U01‐AG46152, P01AG036694)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- CD33, TREM2, TREM-1, Pyk2, monocytes, amyloid pathology
- MeSH terms
- Alzheimer Disease, Amyloid, Humans, Membrane Glycoproteins, Mutation, Receptors, Immunologic, Microglia, Genetic Predisposition to Disease, Sialic Acid Binding Ig-like Lectin 3
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