ReviewInternational journal of molecular sciences2022
Molecular Investigations of Protein Aggregation in the Pathogenesis of Amyotrophic Lateral Sclerosis.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
25 citing papers in PubMed, 36 citations in OpenAlex.
- UA-30 ameliorates motor deficits through RalA-mediated mitophagy in ALS mice.The Journal of clinical investigation · 2026Article
- Consequences of the Novel ALS-AssociatedNeurology. Genetics · 2026Article
- Misfolded Proteins and Cognitive Decline: Mechanistic Insights into Neurodegenerative Disorders.Neurology international · 2026Review
- Mitochondrial and Antioxidant Activity as the Basis of the Neuroprotective Effect of Potential Multitarget Drugs for the Treatment of Neurodegenerative Diseases.Current neuropharmacology · 2026Review
- SOD1, A Crucial Protein for Neural Biochemistry: Dysfunction and Risk of Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2025Review
- Stratifying ALS Patients by Mode of Inheritance Reveals Transcriptomic Signatures Specific to sALS and fALS.International journal of molecular sciences · 2025Article
- Aggregation-Prone Pathogenic SOD1 Variants in Amyotrophic Lateral Sclerosis: Insights from Computational Genomics and Evolutionary Conservation.Journal of molecular neuroscience : MN · 2025Article
- Oxidative Stress in Neurodegenerative Disorders: A Key Driver in Impairing Skeletal Muscle Health.International journal of molecular sciences · 2025Review
- SOD1 Protein Content in Human Central Nervous System and Peripheral Tissues.Journal of neurochemistry · 2025Article
- Targets and Gene Therapy of ALS (Part 1).International journal of molecular sciences · 2025Review
- Role of Antioxidants in Modulating the Microbiota-Gut-Brain Axis and Their Impact on Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Skin pathology in ALS: Diagnostic implications and biomarker potential.Biomolecules & biomedicine · 2025Review
- Mild cognitive impairment in amyotrophic lateral sclerosis: current view.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- The spectrum of behavioral disorders in amyotrophic lateral sclerosis: current view.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Mitochondrial microRNAs: Key Drivers in Unraveling Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Nanoparticles: a new frontier in neurodegenerative disease therapy.Frontiers in medical technology · 2025Review
- Exploring bioactive phytochemicals as ULK1 activators for enhancing cytoprotective autophagy in amyotrophic lateral sclerosis.Frontiers in pharmacology · 2025Article
- Co-Aggregation of TDP-43 with Other Pathogenic Proteins and Their Co-Pathologies in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Rutin Ameliorates ALS Pathology by Reducing SOD1 Aggregation and Neuroinflammation in an SOD1-G93A Mouse Model.International journal of molecular sciences · 2024Article
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a devastating progressive neurodegenerative disorder characterized by selective loss of lower and upper motor neurons (MNs) in the brain and spinal cord, resulting in paralysis and eventually death due to respiratory insufficiency. Although the fundamental physiological mechanisms underlying ALS are not completely understood, the key neuropathological hallmarks of ALS pathology are the aggregation and accumulation of ubiquitinated protein inclusions within the cytoplasm of degenerating MNs. Herein, we discuss recent insights into the molecular mechanisms that lead to the accumulation of protein aggregates in ALS. This will contribute to a better understanding of the pathophysiology of the disease and may open novel avenues for the development of therapeutic strategies.
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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.