ReviewJournal of molecular medicine (Berlin, Germany)2009
Siglec receptors and hiding plaques in Alzheimer's disease.
Review in Journal of molecular medicine (Berlin, Germany), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- 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 Isoform Splicing Dysregulation: A Molecular Determinant of Microglial Dysfunction in Alzheimer's Disease Pathology.Molecular neurobiology · 2026Review
- Neuroinflammation Markers in Tear Fluid of Mild Alzheimer's Disease.Journal of molecular neuroscience : MN · 2025Article
- The role of inhibitory immune checkpoint receptors in the pathogenesis of Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Processing of N-glycans in the ER and Golgi influences the production of surface sialylated glycoRNA.Glycoconjugate journal · 2024Article
- Emerging roles for ITAM and ITIM receptor signaling in microglial biology and Alzheimer's disease-related amyloidosis.Journal of neurochemistry · 2024Review
- Which Moiety Drives Gangliosides to Form Nanodomains?The journal of physical chemistry letters · 2023Article
- Evolution of Human-Specific Alleles Protecting Cognitive Function of Grandmothers.Molecular biology and evolution · 2022Article
- New insights into the genetic etiology of Alzheimer's disease and related dementias.Nature genetics · 2022Article
- Siglecs as Therapeutic Targets in Cancer.Biology · 2021Review
- Sialic Acid-Modified Nanoparticles-New Approaches in the Glioma Management-Perspective Review.International journal of molecular sciences · 2021Review
- Article
- The Paired Siglecs in Brain Tumours Therapy: The Immunomodulatory Effect of Dexamethasone and Temozolomide in Human Glioma In Vitro Model.International journal of molecular sciences · 2021Article
- Reactive or transgenic increase in microglial TYROBP reveals a TREM2-independent TYROBP-APOE link in wild-type and Alzheimer's-related mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Article
- Microglia and its Genetics in Alzheimer's Disease.Current Alzheimer research · 2021Article
- Sialometabolism in Brain Health and Alzheimer's Disease.Frontiers in neuroscience · 2021Review
- Sialic Acid-Siglec Axis as Molecular Checkpoints Targeting of Immune System: Smart Players in Pathology and Conventional Therapy.International journal of molecular sciences · 2020Review
- Lipid and Lipoprotein Metabolism in Microglia.Frontiers in physiology · 2020Review
- The sialoglycan-Siglec-E checkpoint axis in dexamethasone-induced immune subversion in glioma-microglia transwell co-culture system.Immunologic research · 2019Article
- Evaluation of CD33 as a genetic risk factor for Alzheimer's disease.Acta neuropathologica · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease. One hallmark of this disease is the continuous increase in the numbers and size of aggregating amyloid plaques. The accumulation of extracellular plaques is an immunologically interesting phenomenon since microglial cells, brain-specific macrophages, should be able to cleanse the aggregating material from the human brain. Immunotherapy targeting beta-amyloid peptides in plaques with antibodies represents a promising therapy in AD. Recent progress in pattern recognition receptors of monocytes and macrophages has revealed that the sialic acid-binding, immunoglobulin-like lectin (Siglec) family of receptors is an important recognition receptor for sialylated glycoproteins and glycolipids. Interestingly, recent studies have revealed that microglial cells contain only one type of Siglec receptors, Siglec-11, which mediates immunosuppressive signals and thus inhibits the function of other microglial pattern recognition receptors, such as TLRs, NLRs, and RAGE receptors. We will review here the recent literature which clearly indicates that aggregating amyloid plaques are masked in AD by sialylated glycoproteins and gangliosides. Sialylation and glycosylation of plaques, mimicking the cell surface glycocalyx, can activate the immunosuppressive Siglec-11 receptors, as well as hiding the neuritic plaques, allowing them to evade the immune surveillance of microglial cells. This kind of immune evasion can prevent the microglial cleansing process of aggregating amyloid plaques in AD.
Indexed as
Identifiers
What OpenQuestion holds
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.