ArticleNeurobiology of disease2008
A Golgi fragmentation pathway in neurodegeneration.
Article in Neurobiology of disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 140 citations in OpenAlex.
- SIGMA: SIgnaling via Golgi Morphology Analysis for pathway-state classification.bioRxiv : the preprint server for biology · 2026Article
- Golgi dysfunction in Alzheimer disease: from human multiomic signatures to therapeutic targets.Experimental & molecular medicine · 2026Review
- Chondroitin sulfate shapes the unfolded protein response in osteosarcoma to sustain cancer cell survival during ER stress.Cell death & disease · 2026Article
- Glycosylation-driven necroptosis in retinal degeneration: dual rescue by AAV8 gene therapy and RIPK1 inhibition.Cell death discovery · 2026Article
- The Golgi apparatus: adaptations to neuronal shape and functions.The EMBO journal · 2026Review
- The Role of the Golgi Apparatus in Neurodegeneration.Sub-cellular biochemistry · 2026Review
- Organelle-Targeted Nanotherapeutics for Parkinson's Disease: From Pathogenesis to Preclinical Strategies and Translational Challenges.International journal of nanomedicine · 2026Review
- Synphilin-1 modulates alpha-synuclein assembly, release and uptake.NPJ Parkinson's disease · 2025Article
- Neurons and astrocytes have distinct organelle signatures and responses to stress.Cell reports · 2025Article
- Understanding brain calcification via N-terminal acetylation at the Golgi apparatus.Brain : a journal of neurology · 2025Review
- Retrograde transport of neurotrophin receptor TrkB-FL induced by excitotoxicity regulates Golgi stability and is a target for stroke neuroprotection.Cell death & disease · 2025Article
- Distinct Regulation of Early Trafficking of the NMDA Receptors by the Ligand-Binding Domains of the GluN1 and GluN2A Subunits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A genome-wide RNA interference screening reveals protectiveness of SNX5 knockdown in a Parkinson's disease cell model.Translational neurodegeneration · 2025Article
- Cellular Organelle-Related Transcriptomic Profile Abnormalities in Neuronopathic Types of Mucopolysaccharidosis: A Comparison with Other Neurodegenerative Diseases.Current issues in molecular biology · 2024Article
- Emerging Evidence of Golgi Stress Signaling for Neuropathies.Neurology international · 2024Review
- Split but merge: Golgi fragmentation in physiological and pathological conditions.Molecular biology reports · 2024Review
- A transporter's doom or destiny:Frontiers in molecular neuroscience · 2024Review
- Role of Nanoparticle-Conjugates and Nanotheranostics in Abrogating Oxidative Stress and Ameliorating Neuroinflammation.Antioxidants (Basel, Switzerland) · 2023Review
- The function of Golgi apparatus in LRRK2-associated Parkinson's disease.Frontiers in molecular neuroscience · 2023Review
- Contribution of the Golgi apparatus in morphogenesis of a virus-induced cytopathic vacuolar system.Life science alliance · 2022Article
15 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
6 authors at 2 institutions in 1 country.
Funding
Abstract
The Golgi apparatus processes intracellular proteins, but undergoes disassembly and fragmentation during apoptosis in several neurodegenerative disorders such as amyotrophic lateral sclerosis and Alzheimer's disease. It is well known that other cytoplasmic organelles play important roles in cell death pathways. Thus, we hypothesized that Golgi fragmentation might participate in transduction of cell death signals. Here, we found that Golgi fragmentation and dispersal precede neuronal cell death triggered by excitotoxins, oxidative/nitrosative insults, or ER stress. Pharmacological intervention or overexpression of the C-terminal fragment of Grasp65, a Golgi-associated protein, inhibits fragmentation and decreases or delays neuronal cell death. Inhibition of mitochondrial or ER cell death pathways also decreases Golgi fragmentation, indicating crosstalk between organelles and suggesting that the Golgi may be a common downstream-effector of cell death. Taken together, these findings implicate the Golgi as a sensor of stress signals in cell death pathways.
Indexed as
Identifiers
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.