ReviewElectrophoresis2016
Glycosylation and other PTMs alterations in neurodegenerative diseases: Current status and future role in neurotrauma.
Review in Electrophoresis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 64 citations in OpenAlex.
- SGGly: a web server for whole-protein, structure-guided analysis of candidate N-linked glycosylation sites.Nucleic acids research · 2026Article
- DrugPTM-Bench: A Large-Scale Dataset for Predictive Modeling of Drug-Induced Cell Type-Specific Protein Post-Translational Modifications.bioRxiv : the preprint server for biology · 2026Article
- N-Acetylglucosamine Selectively Attenuates Neuroinflammation in a Mouse Model of Mitochondrial Dysfunction.Acta physiologica (Oxford, England) · 2026Article
- PredictiveACS omega · 2026Article
- Deciphering the Glycoproteomic Landscape of Mood Disorders: Unveiling Molecular Association Between CDG and Depression Resilience.Research square · 2025Article
- Post-translational modifications of epigenetic modifier TIP60: their role in cellular functions and cancer.Epigenetics & chromatin · 2025Review
- Exploring the Impact of Mitoquinone Supplementation on Glycan Profiles in a Repeated Mild Traumatic Brain Injury Mouse Model.Neurotrauma reports · 2025Article
- Recent Advances in Labeling-Based Quantitative Glycomics: From High-Throughput Quantification to Structural Elucidation.Proteomics · 2025Review
- Integrating the analysis of human biopsies using post-translational modifications proteomics.Protein science : a publication of the Protein Society · 2024Review
- Recognition ofBiology · 2024Article
- Functions and mechanisms of protein lysine butyrylation (Kbu): Therapeutic implications in human diseases.Genes & diseases · 2023Review
- Glycans as Potential Diagnostic Markers of Traumatic Brain Injury in Children.Diagnostics (Basel, Switzerland) · 2023Article
- ERVW-1 Activates ATF6-Mediated Unfolded Protein Response by Decreasing GANAB in Recent-Onset Schizophrenia.Viruses · 2023Article
- Glycosylation and behavioral symptoms in neurological disorders.Translational psychiatry · 2023Review
- Higher Temperature Porous Graphitic Carbon Separations Differentially Impact Distinct Glycopeptide Classes.Journal of the American Society for Mass Spectrometry · 2023Article
- Advances in neuroproteomics for neurotrauma: unraveling insights for personalized medicine and future prospects.Frontiers in neurology · 2023Review
- Clinical relevance of biomarkers, new therapeutic approaches, and role of post-translational modifications in the pathogenesis of Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- Post-translational Modifications in Parkinson's Disease.Advances in experimental medicine and biology · 2022Article
- Article
- [Large-scale enrichment and identification of human urinarySe pu = Chinese journal of chromatography · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
Traumatic brain injuries (TBIs) present a chief public health threat affecting nations worldwide. As numbers of patients afflicted by TBI are expected to rise, the necessity to increase our understanding of the pathophysiological mechanism(s) as a result of TBI mounts. TBI is known to augment the risk of developing a number of neurodegenerative diseases (NDs) such as Alzheimer's disease (AD) and Parkinson's disease (PD). Hence, it is rational to assume that a common mechanistic ground links the pathophysiology of NDs to that of TBIs. Through this review, we aim to identify the protein-protein interactions, differential proteins expression, and PTMs, mainly glycosylation, that are involved in the pathogenesis of both ND and TBI. OVID and PubMed have been rigorously searched to identify studies that utilized advanced proteomic platforms (MS based) and systems biology tools to unfold the mechanism(s) behind ND in an attempt to unveil the mysterious biological processes that occur postinjury. Various PTMs have been found to be common between TBI and AD, whereas no similarities have been found between TBI and PD. Phosphorylated tau protein, glycosylated amyloid precursor protein, and many other modifications appear to be common in both TBI and AD. PTMs, differential protein profiles, and altered biological pathways appear to have critical roles in ND processes by interfering with their pathological condition in a manner similar to TBI. Advancement in glycoproteomic studies pertaining to ND and TBI is urgently needed in order to develop better diagnostic tools, therapies, and more favorable prognoses.
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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.