ReviewCells2015
Autophagy and Neurodegeneration: Insights from a Cultured Cell Model of ALS.
Review in Cells, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Chromosome 10q24.32 Variants Associate With Brain Arterial Diameters in Diverse Populations: A Genome-Wide Association Study.Journal of the American Heart Association · 2023Pooled it
- A role for mitochondria-ER crosstalk in amyotrophic lateral sclerosis 8 pathogenesis.Life science alliance · 2025Article
- Pexophagy and Oxidative Stress: Focus on Peroxisomal Proteins and Reactive Oxygen Species (ROS) Signaling Pathways.Antioxidants (Basel, Switzerland) · 2025Review
- Chromosome 10q24.32 Variants Associate with Brain Arterial Diameters in Diverse Populations: A Genome-Wide Association Study.medRxiv : the preprint server for health sciences · 2023Article
- Exploring epigenetic drift and rare epivariations in amyotrophic lateral sclerosis by epigenome-wide association study.Frontiers in aging neuroscience · 2023Article
- Proteostasis and neurodegeneration: a closer look at autophagy in Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- Article
- Inflammatory injury and mitophagy of the brain in chicken exposed to Cr(VI).Environmental science and pollution research international · 2021Article
- Review
- Glutathione S-transferase Omega 2 DD genotype is associated with an increased risk of sporadic amyotrophic lateral sclerosis in Chinese men.The Journal of international medical research · 2021Article
- Targeting Beclin1 as an Adjunctive Therapy against HIV Using Mannosylated Polyethylenimine Nanoparticles.Pharmaceutics · 2021Article
- Review
- Expression and role of autophagy related protein p62 and LC3 in the retina in a rat model of acute ocular hypertension.International journal of ophthalmology · 2020Article
- From Multi-Omics Approaches to Precision Medicine in Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2020Review
- Autophagy Activation is Associated with Neuroprotection in Diabetes-associated Cognitive Decline.Aging and disease · 2019Article
- Synchrotron radiation-based FTIR spectro-microscopy of the brainstem of the hSOD1 G93A rat model of amyotrophic lateral sclerosis.European biophysics journal : EBJ · 2019Article
- An open-type microdevice to improve the quality of fluorescence labeling for axonal transport analysis in neurons.Biomicrofluidics · 2019Article
- Deletion of Tbk1 disrupts autophagy and reproduces behavioral and locomotor symptoms of FTD-ALS in mice.Aging · 2019Article
- Repurposing carbamazepine for the treatment of amyotrophic lateral sclerosis in SOD1-G93A mouse model.CNS neuroscience & therapeutics · 2018Article
- Causative Genes in Amyotrophic Lateral Sclerosis and Protein Degradation Pathways: a Link to Neurodegeneration.Molecular neurobiology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy plays a major role in the elimination of cellular waste components, the renewal of intracellular proteins and the prevention of the build-up of redundant or defective material. It is fundamental for the maintenance of homeostasis and especially important in post-mitotic neuronal cells, which, without competent autophagy, accumulate protein aggregates and degenerate. Many neurodegenerative diseases are associated with defective autophagy; however, whether altered protein turnover or accumulation of misfolded, aggregate-prone proteins is the primary insult in neurodegeneration has long been a matter of debate. Amyotrophic lateral sclerosis (ALS) is a fatal disease characterized by selective degeneration of motor neurons. Most of the ALS cases occur in sporadic forms (SALS), while 10%-15% of the cases have a positive familial history (FALS). The accumulation in the cell of misfolded/abnormal proteins is a hallmark of both SALS and FALS, and altered protein degradation due to autophagy dysregulation has been proposed to contribute to ALS pathogenesis. In this review, we focus on the main molecular features of autophagy to provide a framework for discussion of our recent findings about the role in disease pathogenesis of the ALS-linked form of the VAPB gene product, a mutant protein that drives the generation of unusual cytoplasmic inclusions.
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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.