ArticleProceedings of the National Academy of Sciences of the United States of America2014
Aβ-induced Golgi fragmentation in Alzheimer's disease enhances Aβ production.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
What it found
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Who cites it
120 citing papers in PubMed, 194 citations in OpenAlex.
- Golgi dysfunction in Alzheimer disease: from human multiomic signatures to therapeutic targets.Experimental & molecular medicine · 2026Review
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- A role for CASM in the repair of damaged Golgi architecture.Autophagy · 2026Article
- Alu-mediated SPAST deletion impairs golgi zinc transport and reveals a druggable vulnerability.Signal transduction and targeted therapy · 2026Article
- Distinct roles of COPI proteins attenuated in cell senescence.Science advances · 2026Article
- Cholesterol at the Center of Alzheimer's Disease: A Unifying Hypothesis on the Pathogenic Mechanism.Molecules (Basel, Switzerland) · 2026Review
- Multi-ancestry transcriptome-wide association study reveals shared and population-specific genetic effects in Alzheimer disease.American journal of human genetics · 2026Article
- Persistent PirB cleavage drives Golgi-directed trafficking deficits underlying neurodegeneration.Translational neurodegeneration · 2026Article
- Genome-Wide Meta-Analysis for High Myopia Provides Insights into Disease Mechanisms and Reveals a Causal Link to Primary Open-Angle Glaucoma.Ophthalmology science · 2026Article
- Tjap1/Pilt Is a cis-Golgi-Associated Protein Required for Golgi Integrity and Normal Drug Transporter Expression in Brain Microvascular Endothelial Cells In Vitro.Pharmaceutics · 2026Article
- Functional relationships linking C99/APP-βCTF dimerization, proteostasis disruption, and organelle dysfunction.Cell communication and signaling : CCS · 2026Article
- Stress-induced proteome remodeling at the Golgi-endosome interface.Journal of cell science · 2026Article
- Intercompartmental communication in senescence.FEBS open bio · 2026Review
- Spatiotemporal dynamics of reactive oxygen species: implications for cellular homeostasis and redox therapies.Cellular & molecular biology letters · 2026Review
- The Role of the Golgi Apparatus in Neurodegeneration.Sub-cellular biochemistry · 2026Review
- Golgi Fragmentation as a Potential Link Between SARS-CoV-2 Infection and Alzheimer's Disease: Mechanisms and Implications for Neurodegeneration in Long COVID.Sub-cellular biochemistry · 2026Review
- The Dynamic Role of the Golgi Apparatus in Neuronal Function and Alzheimer's Disease.Sub-cellular biochemistry · 2026Review
- The Golgi apparatus: adaptations to neuronal shape and functions.The EMBO journal · 2026Review
- Integrative gene co-expression network analysis reveals protein-coding and LncRNA genes associated with Alzheimer's disease pathology.Scientific reports · 2025Article
- Multi-ancestry Transcriptome-Wide Association Study Reveals Shared and Population-Specific Genetic Effects in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
60 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Golgi fragmentation occurs in neurons of patients with Alzheimer's disease (AD), but the underlying molecular mechanism causing the defects and the subsequent effects on disease development remain unknown. In this study, we examined the Golgi structure in APPswe/PS1E9 transgenic mouse and tissue culture models. Our results show that accumulation of amyloid beta peptides (Aβ) leads to Golgi fragmentation. Further biochemistry and cell biology studies revealed that Golgi fragmentation in AD is caused by phosphorylation of Golgi structural proteins, such as GRASP65, which is induced by Aβ-triggered cyclin-dependent kinase-5 activation. Significantly, both inhibition of cyclin-dependent kinase-5 and expression of nonphosphorylatable GRASP65 mutants rescued the Golgi structure and reduced Aβ secretion by elevating α-cleavage of the amyloid precursor protein. Our study demonstrates a molecular mechanism for Golgi fragmentation and its effects on amyloid precursor protein trafficking and processing in AD, suggesting Golgi as a potential drug target for AD treatment.
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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.