Association of CD33 polymorphism rs3865444 with Alzheimer's disease pathology and CD33 expression in human cerebral cortex
Open accessAbstract
Recent findings identified the minor A allele present in the single-nucleotide polymorphism rs3865444 in the CD33 gene as being associated with the reduced risk of developing Alzheimer's disease (AD). CD33 (Siglec-3) is an immune function protein with anti-inflammatory signaling, cell adhesion, and endocytosis functions with sialic acid-modified proteins or lipids as ligands. Its involvement in AD pathologic mechanisms is still unclear; so, the goal of this study was to investigate if the rs3865444 polymorphism affects the development of AD pathology and the expression of CD33 messenger RNA (mRNA) and protein. For this study, we used DNA from 96 nondemented (ND) and 97 AD neuropathologically diagnosed cases to identify the different rs3865444 alleles and correlate with different measures of AD pathology. Using semiquantitative histologic measures of plaque and tangle pathology, we saw no significant differences between the different genotypes within these disease groups. However, increased expression of CD33 mRNA was associated with increasing AD pathology in temporal cortex brain samples. We also showed that cases with A/A alleles had reduced levels of CD33 protein in temporal cortex but increased levels of the microglia protein IBA-1. Using immunohistochemistry on temporal cortex sections, CD33 was selectively localized to microglia, with greater expression in activated microglia. The factors causing increased CD33 expression by microglia in brain are still unclear, although both genetic and disease factors are involved. Treatment of human microglia isolated from autopsy brains with amyloid-beta peptide and a range of other inflammatory activating agents resulted in reduced CD33 mRNA and protein levels.
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Higher expression of CD33 genes or of CD33 immunolabelled cells was noted in three studies in the superior and middle temporal gyri, frontal cortex and temporal cortex of patients with Alzheimer's disease relative to controls.
“Higher expression of CD33 genes or of CD33 immunolabelled cells was noted in three studies in the superior and middle temporal gyri, frontal cortex and temporal cortex of patients with AD relative to controls.66, 70, 104”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [66]
CD33 expression was shown to correlate with pan-microglial markers Iba1 or CD11b, supporting its microglial localization.
“CD33 expression was shown to correlate with pan-microglial markers Iba1 or CD11b, supporting its microglial localization.66, 70, 104”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [66]
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Self-citation
- Authors
- Walker, D. G., Whetzel, A. M., Serrano, G., Sue, L. I., Beach, T. G., & Lue, L.-F.
- Affiliations
- Banner Sun Health Research Institute (US)
- Corresponding author
- Walker, Douglas G.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2015-02
- Volume
- 36
- Issue
- 2
- Pages
- 571-582
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC4315751
- OpenAlex
- W2148824431
- Cited by
- 93
- References
- 10
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 5 · 2023: 5 · 2022: 10 · 2021: 5 · 2020: 15 · 2019: 15 · 2018: 7 · 2017: 10 · 2016: 5 · 2015: 7
- FWCI
- 4.89
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Arizona Alzheimer's Research Consortium
- Sun Health Foundation
- National Institutes of Health (R21AG034409-A1, R21AG044068-1)
- National Institute of Neurological Disorders and Stroke (U24 NS072026)
- Arizona Department of Health Services
- Arizona Biomedical Research Commission
- Michael J. Fox Foundation for Parkinson's Research
- 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, Alzheimer's disease, genetic polymorphism, microglia, temporal cortex, Iba1, amyloid-beta, neuroinflammation, microglial activation, amyloid plaques, neurofibrillary tangles
- MeSH terms
- Aged, 80 and over, Alleles, Alzheimer Disease, Calcium-Binding Proteins, Cerebral Cortex, DNA-Binding Proteins, Female, Humans, Male, Microfilament Proteins, Risk, RNA, Messenger, Gene Expression, Microglia, Polymorphism, Single Nucleotide, Sialic Acid Binding Ig-like Lectin 3
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