ArticleNeurobiology of aging2015
Association of CD33 polymorphism rs3865444 with Alzheimer's disease pathology and CD33 expression in human cerebral cortex.
Article in Neurobiology of aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.
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Who cites it
59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 91 citations in OpenAlex.
- Markers of microglia in post-mortem brain samples from patients with Alzheimer's disease: a systematic review.Molecular psychiatry · 2018Pooled it
- Associations Between Genetic Variants in 19p13 and 19q13 Regions and Susceptibility to Alzheimer Disease: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2016Pooled it
- CD33 and clusterin interact biophysically and genetically to modulate Alzheimer risk.Nature communications · 2026Article
- Microglial ITAM & ITIM Signaling in Neurodegenerative Disease and Brain Aging.Journal of molecular biology · 2026Review
- Sialylation patterns in cerebral amyloid angiopathy.Brain pathology (Zurich, Switzerland) · 2026Article
- Circulating C-reactive protein influences polygenic risk of inflammatory genes expressed in brain endothelia for Alzheimer's disease.Neurobiology of disease · 2026Article
- Microglia-mediated neuroinflammation in Alzheimer's disease: mechanisms and emerging therapeutic targets.Frontiers in cellular neuroscience · 2026Review
- Coupling relationship between glucose and oxygen metabolisms to serve as an imaging biomarker for Alzheimer's disease.Scientific reports · 2025Article
- Influence of immune cells and inflammatory factors on Alzheimer's disease axis: evidence from mediation Mendelian randomization study.BMC neurology · 2025Article
- The dual role of microglia in Alzheimer's disease: from immune regulation to pathological progression.Frontiers in aging neuroscience · 2025Review
- Cellular and pathological functions of tau.Nature reviews. Molecular cell biology · 2024Review
- Roles in Innate Immunity.Advances in neurobiology · 2024Review
- Advances in the Understanding of the Correlation Between Neuroinflammation and Microglia in Alzheimer's Disease.ImmunoTargets and therapy · 2024Review
- Exploring the Disease-Associated Microglia State in Amyotrophic Lateral Sclerosis.Biomedicines · 2023Article
- Druggable targets for the immunopathy of Alzheimer's disease.RSC medicinal chemistry · 2023Review
- Alzheimer's Disease Treatment: The Search for a Breakthrough.Medicina (Kaunas, Lithuania) · 2023Review
- Increased α-2,6 sialic acid on microglia in amyloid pathology is resistant to oseltamivir.GeroScience · 2023Article
- The impact of increasing levels of blood C-reactive protein on the inflammatory loci SPI1 and CD33 in Alzheimer's disease.Translational psychiatry · 2022Article
- Therapeutics of Alzheimer's Disease: Recent Developments.Antioxidants (Basel, Switzerland) · 2022Review
- Novel Anti-Neuroinflammatory Properties of a Thiosemicarbazone-Pyridylhydrazone Copper(II) Complex.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
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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