ArticleThe FEBS journal2020
Glycan biomarkers for Alzheimer disease correlate with T-tau and P-tau in cerebrospinal fluid in subjective cognitive impairment.
Article in The FEBS journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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
32 citing papers in PubMed, 55 citations in OpenAlex.
- Chemoenzymatic Synthesis of Asymmetric Bisecting Bi-, Tri-, and Tetra-AntennaryJournal of the American Chemical Society · 2025Article
- The emerging landscape of brain glycosylation: from molecular complexity to therapeutic potential.Experimental & molecular medicine · 2025Review
- Deciphering the Glycoproteomic Landscape of Mood Disorders: Unveiling Molecular Association Between CDG and Depression Resilience.Research square · 2025Article
- Cognitive decline in older adults with type 2 diabetes: Unraveling site-specific glycoproteomic alterations.PloS one · 2025Article
- Prevention and Treatment of Alzheimer's Disease Via the Regulation of the Gut Microbiota With Traditional Chinese Medicine.CNS neuroscience & therapeutics · 2024Review
- Clinical glycoproteomics: methods and diseases.MedComm · 2024Review
- Differential expression of N-glycopeptides derived from serum glycoproteins in mild cognitive impairment (MCI) patients.Proteomics · 2024Article
- Recent advances in N-glycan biomarker discovery among human diseases.Acta biochimica et biophysica Sinica · 2024Review
- Integrated Systems Analysis Deciphers Transcriptome and Glycoproteome Links in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
- Native N-glycome profiling of single cells and ng-level blood isolates using label-free capillary electrophoresis-mass spectrometry.Nature communications · 2024Article
- The Cerebrospinal Fluid Free-Glycans HexBiomolecules · 2024Article
- A glycan biomarker predicts cognitive decline in amyloid- and tau-negative patients.Brain communications · 2024Article
- New insight into protein glycosylation in the development of Alzheimer's disease.Cell death discovery · 2023Review
- Presenilin 1 Modulates Acetylcholinesterase Trafficking and Maturation.International journal of molecular sciences · 2023Article
- LC-MS/MS Isomeric Profiling ofBiomolecules · 2022Article
- Systematic synthesis of bisectedChemical science · 2022Article
- The dynamic brain N-glycome.Glycoconjugate journal · 2022Review
- Lack of N-glycosylation increases amyloidogenic processing of the amyloid precursor protein.Glycobiology · 2022Article
- Towards Mapping of the Human Brain N-Glycome with Standardized Graphitic Carbon Chromatography.Biomolecules · 2022Article
- Glycosylation alterations in serum of Alzheimer's disease patients show widespread changes inAlzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer disease (AD) is a devastating disease and a global health problem, and current treatments are only symptomatic. A wealth of clinical studies support that the disease starts to develop decades before the first symptoms appear, emphasizing the importance of studying early changes for improving early diagnosis and guiding toward novel treatment strategies. Protein glycosylation is altered in AD but it remains to be clarified why these alterations occur and how they affect the disease development. Here, we used a glycomics approach to search for alterations in protein glycosylation in cerebrospinal fluid (CSF) in AD compared with nondemented controls. Using both matrix-assisted laser desorption ionization-time of flight and liquid chromatography-electrospray mass spectrometry, we observed an increase in N-glycans carrying bisecting N-acetylglucosamine in AD. Based on those findings, we designed an enzyme-linked multiwell plate assay to quantify N-glycans binding to the lectin Phaseolus vulgaris Erythroagglutinin (PHA-E), which is specific for N-glycans containing bisecting N-acetylglucosamine. Using this assay, we found a similar increase in CSF in AD compared with controls. Further analysis of CSF from 242 patients with subjective cognitive impairment (SCI), mild cognitive impairment (MCI), or AD dementia revealed significantly increased binding to PHA-E in MCI and AD compared to SCI. Interestingly, PHA-E binding correlated with CSF levels of phosphorylated tau and total tau and this correlation was most prominent in the SCI group (R = 0.53-0.54). This study supports a link between N-glycosylation, neurodegeneration, and tau pathology in AD and suggests that glycan biomarkers have potential to identify SCI cases at risk of developing 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.