ReviewACS omega2026
Landscape of Protein Post-Translational Modifications in Age-Related Neurodegenerative Disorders: Implications in Protein Aggregation, Altered Cellular Processes, and Therapeutics.
Review in ACS omega, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Nascent protein retention at polysomes reduces kinetic barriers to self-assembly.bioRxiv : the preprint server for biology · 2026Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of aggregated or nonfunctional proteins during the aging process is a common hallmark of degenerating neurons in various neurodegenerative disorders. Post-translational modifications (PTMs) such as acetylation, methylation, phosphorylation, and ubiquitination, etc. in combination with the protein quality control machinery such as autophagy and proteasome systems are essential for the degradation of these toxic aggregates, to maintain normal protein turnover and function of neurons. Abnormal protein quality control machinery primarily mediated by altered post-translational modifications of various proteins are linked to neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and many others. Accumulating evidence from the past two decades shows that targeting these PTMs with various small molecule activators or inhibitors restores synaptic and cognitive processes associated with these neurodegenerative diseases. Here, in this review, we highlight how these PTMs affect the accumulation and aggregation of nonfunctional proteins in various neurodegenerative diseases. Also, we highlight the current advances in exploring small molecule modulators of modifying enzymes as therapeutic options for these diseases.
Identifiers
What Socratic 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 Socratic graph.