ReviewCell & bioscience2024
Abnormal protein post-translational modifications induces aggregation and abnormal deposition of protein, mediating neurodegenerative diseases.
Review in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- The effects of traditional mind-body exercises on cognitive function in neurodegenerative diseases or prodromal cognitive decline: a meta-analysis.Frontiers in public health · 2026Pooled it
- Artificial Intelligence for Alzheimer's Disease Diagnosis: From Traditional Machine Learning to Large Language Models.Biosensors · 2026Review
- Large-scale single-molecule analysis of tau proteoforms.Nature methods · 2026Article
- Post-translational modifications in the brain are critical contributors to Alzheimer's disease neuropathology and cognitive decline.bioRxiv : the preprint server for biology · 2026Article
- AGGRESCAN and its evolution: A two-decade perspective on protein aggregation prediction.Biophysical reviews · 2026Review
- Molecular and cellular processes connecting type 2 diabetes to Alzheimer's disease, focusing on oxidative stress, metabolic dysfunction, and neurodegeneration.Genetics and molecular biology · 2026Article
- Unlocking the Sugar Code: Implications and Consequences of Glycosylation in Alzheimer's Disease and Other Tauopathies.Biomedicines · 2025Review
- Implications of Mucin-TypeMolecules (Basel, Switzerland) · 2025Review
- Role of Oxidative Stress in Blood-Brain Barrier Disruption and Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- ST8Sia2 polysialyltransferase protects against infection by Trypanosoma cruzi.PLoS neglected tropical diseases · 2024Article
- Protein modification in neurodegenerative diseases.MedComm · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Protein post-translational modifications (PPTMs) refer to a series of chemical modifications that occur after the synthesis of protein. Proteins undergo different modifications such as phosphorylation, acetylation, ubiquitination, and so on. These modifications can alter the protein's structure, function, and interaction, thereby regulating its biological activity. In neurodegenerative diseases, several proteins undergo abnormal post-translational modifications, which leads to aggregation and abnormal deposition of protein, thus resulting in neuronal death and related diseases. For example, the main pathological features of Alzheimer's disease are the aggregation of beta-amyloid protein and abnormal phosphorylation of tau protein. The abnormal ubiquitination and loss of α-synuclein are related to the onset of Parkinson's disease. Other neurodegenerative diseases such as Huntington's disease, amyotrophic lateral sclerosis, and so on are also connected with abnormal PPTMs. Therefore, studying the abnormal PPTMs in neurodegenerative diseases is critical for understanding the mechanism of these diseases and the development of significant therapeutic strategies. This work reviews the implications of PPTMs in neurodegenerative diseases and discusses the relevant therapeutic strategies.
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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 Socratic graph.