ReviewCells2017
Assessment of Autophagy in Neurons and Brain Tissue.
Review in Cells, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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, 52 citations in OpenAlex.
- Autophagy in Alzheimer's Disease: Mechanisms, Clinical Trials, and Horizons.Neuro-degenerative diseases · 2026Review
- Chaperone mediated autophagy is deficient in spinal motoneurons of ALS patients with TDP-43 proteinopathy.Acta neuropathologica communications · 2026Article
- Impact of Hericium erinaceus and Ganoderma lucidum metabolites on AhR activation in neuronal HT-22 cells.Pharmacological reports : PR · 2025Article
- Article
- Regulation of the innate immune response in human neurons by ICP34.5 maintains herpes simplex virus 1 latency.bioRxiv : the preprint server for biology · 2025Article
- Proteomics and Expression of HIF2α/BNIP3L Signaling in Yak Brains at Different Altitudes.International journal of molecular sciences · 2025Article
- Autophagy, a double-edged sword for oral tissue regeneration.Journal of advanced research · 2024Review
- Regulated cell death and its role in Alzheimer's disease and amyotrophic lateral sclerosis.Acta neuropathologica · 2024Review
- Spinal cord abnormal autophagy and mitochondria energy metabolism are modified by swim training in SOD1-G93A mice.Journal of molecular medicine (Berlin, Germany) · 2024Article
- A crosstalk between autophagy and apoptosis in intracerebral hemorrhage.Frontiers in cellular neuroscience · 2024Review
- Insulin Inhibits Autophagy by Inhibiting the Binding of FoXO1 to the Promoter Region of GABARAPL1.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2023Article
- High glucose inhibits neural differentiation by excessive autophagy <em>via</em> peroxisome proliferator-activated receptor gamma.European journal of histochemistry : EJH · 2023Article
- Impaired Autophagic-Lysosomal Fusion in Parkinson's Patient Midbrain Neurons Occurs through Loss of ykt6 and Is Rescued by Farnesyltransferase Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Modulating autophagic flux via ROS-responsive targeted micelles to restore neuronal proteostasis in Alzheimer's disease.Bioactive materials · 2022Article
- Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?Frontiers in cellular neuroscience · 2022Review
- Insights Into the Role of Platelet-Derived Growth Factors: Implications for Parkinson's Disease Pathogenesis and Treatment.Frontiers in aging neuroscience · 2022Review
- Neuronal Autophagy: Characteristic Features and Roles in Neuronal Pathophysiology.Biomolecules & therapeutics · 2021Review
- ATM loss disrupts the autophagy-lysosomal pathway.Autophagy · 2021Article
- AMPK activation does not enhance autophagy in neurons in contrast to MTORC1 inhibition: different impact on β-amyloid clearance.Autophagy · 2021Article
- Spatiotemporal analysis of soluble aggregates and autophagy markers in the R6/2 mouse model.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a complex process that controls the transport of cytoplasmic components into lysosomes for degradation. This highly conserved proteolytic system involves dynamic and complex processes, using similar molecular elements and machinery from yeast to humans. Moreover, autophagic dysfunction may contribute to a broad spectrum of mammalian diseases. Indeed, in adult tissues, where the capacity for regeneration or cell division is low or absent (e.g., in the mammalian brain), the accumulation of proteins/peptides that would otherwise be recycled or destroyed may have pathological implications. Indeed, such changes are hallmarks of pathologies, like Alzheimer's, Prion or Parkinson's disease, known as proteinopathies. However, it is still unclear whether such dysfunction is a cause or an effect in these conditions. One advantage when analysing autophagy in the mammalian brain is that almost all the markers described in different cell lineages and systems appear to be present in the brain, and even in neurons. By contrast, the mixture of cell types present in the brain and the differentiation stage of such neurons, when compared with neurons in culture, make translating basic research to the clinic less straightforward. Thus, the purpose of this review is to describe and discuss the methods available to monitor autophagy in neurons and in the mammalian brain, a process that is not yet fully understood, focusing primarily on mammalian macroautophagy. We will describe some general features of neuronal autophagy that point to our focus on neuropathologies in which macroautophagy may be altered. Indeed, we centre this review around the hypothesis that enhanced autophagy may be able to provide therapeutic benefits in some brain pathologies, like Alzheimer's disease, considering this pathology as one of the most prevalent proteinopathies.
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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.