ReviewThe Lancet. Neurology2018
Selective autophagy as a potential therapeutic target for neurodegenerative disorders.
Review in The Lancet. Neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 4 of them syntheses 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
200 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- Retinal Pigment Epithelium Phagocytosis and Retinal Degenerative Diseases.Aging and disease · 2025Pooled it
- Targeting Protein Aggregates with Natural Products: An Optional Strategy for Neurodegenerative Diseases.International journal of molecular sciences · 2023Pooled it
- Systematic review and meta-analysis of human transcriptomics reveals neuroinflammation, deficient energy metabolism, and proteostasis failure across neurodegeneration.Neurobiology of disease · 2021Pooled it
- Pooled it
- Neuron-derived extracellular vesicles to examine brain mTOR target engagement with sirolimus in patients with multiple system atrophy.Parkinsonism & related disorders · 2023Trial
- mTOR Inhibition with Sirolimus in Multiple System Atrophy: A Randomized, Double-Blind, Placebo-Controlled Futility Trial and 1-Year Biomarker Longitudinal Analysis.Movement disorders : official journal of the Movement Disorder Society · 2022Trial
- Targeting Mitochondria for Postoperative Cognitive Dysfunction: From Mechanisms to Therapeutics.Molecular neurobiology · 2026Review
- Assessment of apoptosis and autophagy in oral squamous cell carcinoma cell line treated with salivary exosomes.Odontology · 2026Article
- Small bites for big problems: stepwise aggregate degradation by autophagy.Biochemical Society transactions · 2026Review
- Surface microstructures of tricalcium phosphate regulate the autophagy of osteoclasts through the MAPK/ERK signaling pathway.Journal of materials science. Materials in medicine · 2026Article
- Cognitive-Enhancing Effects of Bioactive Compounds and Traditional Herbal Medicines in Elderly Patients with Metabolic Syndrome.Biomolecules · 2026Review
- The Fragile Balance: Autophagy's Role in Neurodegenerative Disease Progression.Current neuropharmacology · 2026Review
- Programmed Cell Death: A Key Mechanism of Traditional Chinese Medicine in the Treatment of Membranous Nephropathy.Drug design, development and therapy · 2026Review
- Deciphering the Neuroautophagic Interactome: Molecular Circuits Linking Selective Autophagy to Neuropathological Cascades in Neurological Disorders.International journal of biological sciences · 2026Review
- Oral Exposure to Food-Grade Nanoparticles Poses a Risk of Alzheimer's Disease-Like Symptoms by Triggering Autophagy Defects in Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spermine modulation of Alzheimer's Tau and Parkinson's α-synuclein: implications for biomolecular condensation and neurodegeneration.Nature communications · 2025Article
- Microglia-derived nanovesicles synchronize macroautophagy and chaperone-mediated autophagy for Alzheimer's disease therapy.Signal transduction and targeted therapy · 2025Article
- Research Advances of the Autophagy-Regulated Radiosensitivity.Cell proliferation · 2025Review
- A chaperone-proteasome-based fragmentation machinery is essential for aggrephagy.Nature cell biology · 2025Article
- Recombinant cathepsins B and L promote α-synuclein clearance and restore lysosomal function in human and murine models with α-synuclein pathology.Molecular neurodegeneration · 2025Article
140 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
4 authors.
Funding
Abstract
Cells rely on surveillance systems such as autophagy to handle protein alterations and organelle damage. Dysfunctional autophagy, an evolutionarily conserved cellular mechanism for degradation of intracellular components in lysosomes, frequently leads to neurodegeneration. The neuroprotective effect of autophagy stems from its ability to eliminate pathogenic forms of proteins such as α-synuclein or tau. However, the same pathogenic proteins often affect different types and steps of the autophagic process. Furthermore, genetic studies have shown that some proteins related to neurodegeneration, such as huntingtin, participate in autophagy as one of their physiological functions. This complex interplay between autophagy and neurodegeneration suggests that targeting autophagy as a whole might have limited applicability in neurodegenerative diseases, and that future efforts should focus instead on targeting specific types and steps of the autophagic process. This change of strategy in the modulation of autophagy might hold promise for future disease-modifying therapies for patients with neurodegenerative disorders.
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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.