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CD33 Alzheimer's disease locus: altered monocyte function and amyloid biology
Open accessAbstract
In our functional dissection of the CD33 Alzheimer's disease susceptibility locus, we found that the rs3865444(C) risk allele was associated with greater cell surface expression of CD33 in the monocytes (t50 = 10.06, P(joint) = 1.3 × 10(-13)) of young and older individuals. It was also associated with diminished internalization of amyloid-β 42 peptide, accumulation of neuritic amyloid pathology and fibrillar amyloid on in vivo imaging, and increased numbers of activated human microglia.
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“At the genetic level, GWAS and sequencing studies have found associations between AD and genes expressed in myeloid cells, including TREM2, ABCA7, and CD331,2,5,15–17.”
From A common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease (2017) · cites this paper as [17]
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“Limited clearance by microglia is likely to contribute to increased Ab 1 -42 burden in the brains of sporadic AD dementia patients, as described recently for the CD33 risk allele rs3865444 (13).”
From SUCLG2 identified as both a determinator of CSF Aβ1–42 levels and an attenuator of cognitive decline in Alzheimer's disease (2014) · cites this paper as [13]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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 [17]
The cited source says what the claim attributes to it.
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“The AD-associated risk allele of CD33 likely produces the longer more active spliced form of this inhibitory receptor (Pimenova et al., 2017b), which correlates with increased cell surface expression and reduced phagocytic capacity observed in human monocytes (Bradshaw et al., 2013).”
From Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response (2021) · cites this paper as Bradshaw et al., 2013
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In the citing paper
“Two polymorphisms in the CD33 gene have recently been identified that modulate AD risk,102, 103 with the protective allele associated with reduced CD3312, 66, 70 and increased phagocytosis.12”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [12]
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“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 [34]
In the citing paper
“a CD33 variant associated with an increased risk for AD is expressed at relatively high levels, increasing CD33 inhibitory effects on myeloid functions, such as internalization of the Aβ1–42 peptide (137).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [137]
In the citing paper
“The CD33 genotype–phenotype relationship nicely aligns with that of TREM2: the TREM2 R47H mutation (which increases AD risk) reduces TREM2–ligand binding and ITAM signaling and impairs phagocytosis, whereas the CD33 variant (which reduces AD risk) prevents the CD33–ligand interaction and presumably ITIM signaling and promotes phagocytosis (Bradshaw et al., 2013; Griciuc et al., 2013).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Bradshaw et al., 2013
In the citing paper
“Genetic studies show that a number of genes that have been linked to early-onset AD risk are expressed primarily in microglia.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [134]
In the citing paper
“Since most GWAS loci are thought to operate by regulating the expression of neighbouring genes (Bradshaw et al., 2013; Griciuc et al., 2013; Huang et al., 2017)”
From Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk (2019) · cites this paper as Bradshaw et al., 2013
In the citing paper
“These findings are also consistent with previous work on Trem2 (Wang et al., 2015; Keren-Shaul et al., 2017; Mazaheri et al., 2017; Cheng-Hathaway et al., 2018; Lee et al., 2018), and CD33 (Bradshaw et al., 2013; Griciuc et al., 2013), suggesting these risk genes are crucial in controlling the microglial response to amyloid-induced damage.”
From Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk (2019) · cites this paper as Bradshaw et al., 2013
In the citing paper
“Whereas cells exposed to these two factors responded differentially to fAβ, increasing expression of genes involved in neuronal cell surface motif recognition, or phagocytosis of CNS substrates, including MS4A genes, TREM2, TYROBP, CD33, and ABCA7 (Bradshaw et al., 2013; Fu et al., 2016; Greer et al., 2016)(Figure S6B).”
From iPSC-derived human microglia-like cells to study neurological diseases (2017) · cites this paper as Bradshaw et al., 2013
In the citing paper
“genes previously implicated in modulating Aβ phagocytosis and clearance”
From iPSC-derived human microglia-like cells to study neurological diseases (2017) · cites this paper as Bradshaw et al., 2013
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Metadata
- Authors
- Initiative, T. A. D. N., Bradshaw, E. M., Chibnik, L. B., Keenan, B. T., Ottoboni, L., Raj, T., Tang, A., Rosenkrantz, L. L., Imboywa, S., Lee, M., Von Korff, A., Morris, M. C., Evans, D. A., Johnson, K., Sperling, R. A., Schneider, J. A., Bennett, D. A., & De Jager, P. L.
- Affiliations
- Brigham and Women's Hospital (US)
- Broad Institute (US)
- Rush University Medical Center (US)
- Harvard University (US)
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2013-05-23
- Volume
- 16
- Issue
- 7
- Pages
- 848-850
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC3703870
- OpenAlex
- W2074405990
- Cited by
- 570
- References
- 41
- Citations by year
- 2026: 9 · 2025: 30 · 2024: 56 · 2023: 48 · 2022: 42 · 2021: 45 · 2020: 53 · 2019: 59 · 2018: 49 · 2017: 46 · 2016: 41 · 2015: 49 · 2014: 32 · 2013: 11
- FWCI
- 30.79
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- National Institute on Aging (R01AG017917, P30-AG 10161, K25AG041906, R01AG030146, R01 AG30146, R01‐AG17917, R01 AG15819, R01AG11101, P50AG005138, R01AG011101, R01AG036042, R01AG043617, R01AG015819, P30AG010161, P30AG008051, P50AG008702, P30AG013846, R01AG031553, U24AG021886)
- National Institute of General Medical Sciences (R25GM076321, RC2GM093080)
- National Institute of Neurological Disorders and Stroke (R10 NS067305, R01NS067305)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, Alzheimer's disease, genetic susceptibility loci, monocytes, microglial activation, amyloid-beta, amyloid fibrils, cell surface expression
- MeSH terms
- Adult, Age Factors, Aged, Aged, 80 and over, Alzheimer Disease, Aniline Compounds, Brain, Dextrans, Female, Genotype, HLA-D Antigens, Humans, Male, Middle Aged, Monocytes, Peptide Fragments, Polymorphism, Genetic, Radionuclide Imaging, Thiazoles, Cohort Studies, Amyloid beta-Peptides, Microglia, Young Adult, Genetic Association Studies, Plaque, Amyloid, Cognitive Dysfunction, Sialic Acid Binding Ig-like Lectin 3
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