ReviewMolecular brain2019
Autophagic and endo-lysosomal dysfunction in neurodegenerative disease.
Review in Molecular brain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 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
116 citing papers in PubMed, 185 citations in OpenAlex.
- The GBA1-related variant rs12411216 is Associated with Motor and Non-Motor Impairments and Unfavorable Progression in Parkinson's Disease: A Five-Year Longitudinal Study.Journal of molecular neuroscience : MN · 2026Article
- Applying a systemic approach that extends beyond the brain to Alzheimer's disease pathogenesis.Communications medicine · 2026Article
- Article
- From synaptic development to degeneration: a narrative review of small molecule strategies targeting alpha-synuclein in Parkinson's disease.Metabolic brain disease · 2026Review
- Late Endosome Transport by RILP-RAB7A Promotes Dendrite Arborization Independently of Degradation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Functional relationships linking C99/APP-βCTF dimerization, proteostasis disruption, and organelle dysfunction.Cell communication and signaling : CCS · 2026Article
- Acetylation of STX17 promotes its autophagosomal translocation.Nature communications · 2026Article
- Cystatin F as a neuroimmune effector in CNS inflammation and neurodegeneration.Frontiers in cell and developmental biology · 2026Review
- Molecular mechanisms of autophagy-lysosomal pathway dysfunction in neurodegenerative diseases and therapeutic strategies for lysosomal repair: a review.Frontiers in neuroscience · 2026Review
- Lysosome trafficking across intracellular and intercellular networks in the brain.Frontiers in molecular neuroscience · 2026Article
- Extracellular Mitochondrial Components as Emerging Biomarkers and Therapeutic Targets in Human Diseases.International journal of biological sciences · 2026Review
- Exploring the Potential of Herbal Compounds as Autophagy Modulators in Alzheimer's Disease: A Comprehensive Review.CNS & neurological disorders drug targets · 2026Review
- Late endosome transport by RILP-RAB7A promotes dendrite arborization.bioRxiv : the preprint server for biology · 2025Article
- Proteomic analysis links truncated tau to lysosome motility, autophagy, and endo-lysosomal dysfunction.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Chr:17q21.31 locus risk haplotype H1 susceptibility to ferroptosis is mediated by endolysosomal pathway.Cell death & disease · 2025Article
- Article
- Sequelae and reversal of age-dependent alterations in mitochondrial dynamics via autophagy enhancement in reprogrammed human neurons.bioRxiv : the preprint server for biology · 2025Article
- Disruption of ClC-3-mediated 2ClScientific reports · 2025Article
- Lysosomal Network Defects in Early-Onset Parkinson's Disease Patients Carrying Rare Variants in Lysosomal Hydrolytic Enzyme Genes.International journal of molecular sciences · 2025Article
- Progress in Disease-Modifying Therapies for Parkinson's Disease.Aging and disease · 2025Review
56 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 at 1 institution in 1 country.
Funding
Abstract
Due to their post-mitotic state, metabolic demands and often large polarised morphology, the function and survival of neurons is dependent on an efficient cellular waste clearance system both for generation of materials for metabolic processes and removal of toxic components. It is not surprising therefore that deficits in protein clearance can tip the balance between neuronal health and death. Here we discuss how autophagy and lysosome-mediated degradation pathways are disrupted in several neurological disorders. Both genetic and cell biological evidence show the diversity and complexity of vesicular clearance dysregulation in cells, and together may ultimately suggest a unified mechanism for neuronal demise in degenerative conditions. Causative and risk-associated mutations in Alzheimer's disease, Frontotemporal Dementia, Amyotrophic Lateral Sclerosis, Parkinson's disease, Huntington's disease and others have given the field a unique mechanistic insight into protein clearance processes in neurons. Through their broad implication in neurodegenerative diseases, molecules involved in these genetic pathways, in particular those involved in autophagy, are emerging as appealing therapeutic targets for intervention in neurodegeneration.
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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.