ReviewCell communication and signaling : CCS2024
Misfolding and aggregation in neurodegenerative diseases: protein quality control machinery as potential therapeutic clearance pathways.
Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 1 synthesis or guideline pooled it.
- 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
- Oxidative stress and inflammation in neurodegenerative disorders.Archives of toxicology · 2026Review
- Genes near tRNAs are enriched in translational machinery.G3 (Bethesda, Md.) · 2026Article
- Distinct single-nucleus RNA-seq changes among non-neuronal cells in ADNC, LATE-NC, and mixed pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Advances in ultrasound-mediated nanozyme systems in therapeutic applications.Ultrasonics sonochemistry · 2026Review
- Neurons Die Not by One Hit, but by Signaling Convergence.Molecular neurobiology · 2026Review
- Review
- Reimagining the contribution of iron in Parkinson's disease.Neurobiology of disease · 2026Review
- CPEB3 selectively inhibits α-synuclein aggregation without modulating TDP-43 pathology.FEBS letters · 2026Article
- Network Biology of Alzheimer's Disease and Related Neurodegenerative Disorders: Molecular Mechanisms and Therapeutic Strategies.Biomolecules · 2026Review
- Systematic Mapping of Protein Interactions Underlying IL-2 Secretion in Human T Cells.Analytical chemistry · 2026Article
- DJ-1 in the Neuro-cutaneous Aging Axis: Unifying Pathways of Parkinson's Disease Neurodegeneration, Progression, and Redox-Based Therapeutic Strategies for Healthy Longevity.Molecular neurobiology · 2026Review
- Tracing the threads: How toxic metals contribute to neurodegeneration.IBRO neuroscience reports · 2026Review
- Copper Coordination to the Prion Fragment (95-126): Implications for Neurodegenerative Diseases.International journal of molecular sciences · 2026Article
- The Oxidative Stress: Origin and Role in Aging and Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondria serve as a holdout compartment for aggregation-prone proteins hindering efficient degradation.Nature communications · 2026Article
- FTDP-17T Mutations Promote Formation of Phosphorylated FTDP-17T TAU Oligomers That Cause Degeneration of Dopaminergic and Hippocampal Neurons via Activating ER Stress and Mitochondrial Pro-apoptotic Cascades.Neurochemical research · 2026Article
- Biochemical Mechanisms of Cellular Stress Adaptation in the Pathogenesis of Chronic Diseases.Molecules (Basel, Switzerland) · 2026Review
- Plant-Derived Peptides with Neuroprotective Activity: Advances and Perspectives in the Prevention of Neurodegenerative Diseases.ACS omega · 2026Review
- Top-Down Mass Spectrometry and Its Current Applications in Biomarker Discovery in Aging and Age-Related Diseases.International journal of molecular sciences · 2026Review
7 more citing papers are in PubMed but not listed here.
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
Abstract
The primary challenge in today's world of neuroscience is the search for new therapeutic possibilities for neurodegenerative disease. Central to these disorders lies among other factors, the aberrant folding, aggregation, and accumulation of proteins, resulting in the formation of toxic entities that contribute to neuronal degeneration. This review concentrates on the key proteins such as β-amyloid (Aβ), tau, and α-synuclein, elucidating the intricate molecular events underlying their misfolding and aggregation. We critically evaluate the molecular mechanisms governing the elimination of misfolded proteins, shedding light on potential therapeutic strategies. We specifically examine pathways such as the endoplasmic reticulum (ER) and unfolded protein response (UPR), chaperones, chaperone-mediated autophagy (CMA), and the intersecting signaling of Keap1-Nrf2-ARE, along with autophagy connected through p62. Above all, we emphasize the significance of these pathways as protein quality control mechanisms, encompassing interventions targeting protein aggregation, regulation of post-translational modifications, and enhancement of molecular chaperones and clearance. Additionally, we focus on current therapeutic possibilities and new, multi-target approaches. In conclusion, this review systematically consolidates insights into emerging therapeutic strategies predicated on protein aggregates clearance.
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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.