ReviewActa neuropathologica2019
Evaluation of CD33 as a genetic risk factor for Alzheimer's disease.
Review in Acta neuropathologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Microglial Phagocytosis: A Disease-Associated Process Emerging from Alzheimer's Disease Genetics.Trends in neurosciences · 2020Pooled it
- CD33 and clusterin interact biophysically and genetically to modulate Alzheimer risk.Nature communications · 2026Article
- Crystal structure of the CD33/Fab-10C8 complex elucidates the mechanism of antibody antagonism in HBV-induced immunosuppression.Journal of biomedical science · 2026Article
- Article
- CD33 Isoform Splicing Dysregulation: A Molecular Determinant of Microglial Dysfunction in Alzheimer's Disease Pathology.Molecular neurobiology · 2026Review
- Immunomodulation by glycosylation: bridging glycobiology to adaptive immunity and therapeutic innovation.Frontiers in immunology · 2026Review
- Translating Alzheimer's Disease Mechanisms into Therapeutic Opportunities.Biomolecules · 2025Review
- SerumJournal of proteome research · 2025Article
- Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions.Molecular neurodegeneration · 2025Review
- Celebrating 40 years of the University of Kentucky Alzheimer's Disease Research Center.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Unique N-glycosylation signatures in human iPSC derived microglia activated by Aβ oligomer and lipopolysaccharide.Scientific reports · 2025Article
- CD33-D2 isoform characterization for advancement of its therapeutic potential.Immunotherapy · 2025Article
- Influence of immune cells and inflammatory factors on Alzheimer's disease axis: evidence from mediation Mendelian randomization study.BMC neurology · 2025Article
- CD33 Ameliorates Surgery-Induced Spatial Learning and Memory Impairments Through TREM2.Molecular neurobiology · 2025Article
- CRISPR/Cas9-Based therapeutics as a promising strategy for management of Alzheimer's disease: progress and prospects.Frontiers in cellular neuroscience · 2025Review
- TREM2Frontiers in immunology · 2025Review
- The role of inhibitory immune checkpoint receptors in the pathogenesis of Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Article
- HuM195 and its single-chain variable fragment increase Aβ phagocytosis in microglia via elimination of CD33 inhibitory signaling.Molecular psychiatry · 2024Article
- Alzheimer's disease associated isoforms of human CD33 distinctively modulate microglial cell responses in 5XFAD mice.Molecular neurodegeneration · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In 2011, genome-wide association studies implicated a polymorphism near CD33 as a genetic risk factor for Alzheimer's disease. This finding sparked interest in this member of the sialic acid-binding immunoglobulin-type lectin family which is linked to innate immunity. Subsequent studies found that CD33 is expressed in microglia in the brain and then investigated the molecular mechanism underlying the CD33 genetic association with Alzheimer's disease. The allele that protects from Alzheimer's disease acts predominately to increase a CD33 isoform lacking exon 2 at the expense of the prototypic, full-length CD33 that contains exon 2. Since this exon encodes the sialic acid ligand-binding domain, the finding that the loss of exon 2 was associated with decreased Alzheimer's disease risk was interpreted as meaning that a decrease in functional CD33 and its associated immune suppression was protective from Alzheimer's disease. However, this interpretation may need to be reconsidered given current findings that a genetic deletion which abrogates CD33 is not associated with Alzheimer's disease risk. Therefore, integrating currently available findings leads us to propose a model wherein the CD33 isoform lacking the ligand-binding domain represents a gain of function variant that reduces Alzheimer's disease risk.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.