ArticleNeurobiology of disease2017
Morphometric alterations of Golgi apparatus in Alzheimer's disease are related to tau hyperphosphorylation.
Article in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Catecholamines in Alzheimer's Disease: A Systematic Review and Meta-Analysis.Frontiers in aging neuroscience · 2020Pooled it
- Golgi dysfunction in Alzheimer disease: from human multiomic signatures to therapeutic targets.Experimental & molecular medicine · 2026Review
- The Role of the Golgi Apparatus in Neurodegeneration.Sub-cellular biochemistry · 2026Review
- The Golgi apparatus: adaptations to neuronal shape and functions.The EMBO journal · 2026Review
- Organelle perturbation in Alzheimer's disease: do intracellular amyloid-ß and the fragmented Golgi mediate early intracellular neurotoxicity?Frontiers in cell and developmental biology · 2025Review
- Updates in Alzheimer's disease: from basic research to diagnosis and therapies.Translational neurodegeneration · 2024Review
- An automated high-content screening and assay platform for the analysis of spheroids at subcellular resolution.PloS one · 2024Article
- Secretagogin as a marker to distinguish between different neuron types in human frontal and temporal cortex.Frontiers in neuroanatomy · 2023Article
- Golgi fragmentation - One of the earliest organelle phenotypes in Alzheimer's disease neurons.Frontiers in neuroscience · 2023Article
- Progression of Alzheimer's disease parallels unusual structural plasticity of human dentate granule cells.Acta neuropathologica communications · 2022Article
- Pyramidal cell axon initial segment in Alzheimer´s disease.Scientific reports · 2022Article
- Therapeutic Targeting of Rab GTPases: Relevance for Alzheimer's Disease.Biomedicines · 2022Review
- Small GTPases of the Rab and Arf Families: Key Regulators of Intracellular Trafficking in Neurodegeneration.International journal of molecular sciences · 2021Review
- Differential expression of secretagogin immunostaining in the hippocampal formation and the entorhinal and perirhinal cortices of humans, rats, and mice.The Journal of comparative neurology · 2020Article
- Review
- Tau Secretion: Good and Bad for Neurons.Frontiers in neuroscience · 2019Review
- Golgi Complex Dynamics and Its Implication in Prevalent Neurological Disorders.Frontiers in cell and developmental biology · 2019Review
- The Golgi Apparatus of Neocortical Glial Cells During Hibernation in the Syrian Hamster.Frontiers in neuroanatomy · 2019Article
- Inactivation of NSF ATPase Leads to Cathepsin B Release After Transient Cerebral Ischemia.Translational stroke research · 2018Article
- Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease.Brain : a journal of neurology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Golgi apparatus (GA) is a highly dynamic organelle, which is mainly involved in the post-translational processing and targeting of cellular proteins and which undergoes significant morphological changes in response to different physiological and pathological conditions. In the present study, we have analyzed the possible alterations of GA in neurons from the temporal neocortex and hippocampus of Alzheimer's disease (AD) patients, using double immunofluorescence techniques, confocal microscopy and 3D quantification techniques. We found that in AD patients, the percentage of temporal neocortical and CA1 hippocampal pyramidal neurons with a highly altered GA is much higher (approximately 65%) in neurons with neurofibrillary tangles (NFT) than in NFT-free neurons (approximately 6%). Quantitative analysis of the surface area and volume of GA elements in neurons revealed that, compared with NFT-free neurons, NFT-bearing neurons had a reduction of approximately one half in neocortical neurons and one third in CA1 neurons. In both regions, neurons with a pre-tangle stage of phospho-tau accumulation had surface area and GA volume values that were intermediate, that is, between those of NFT-free and NFT-bearing neurons. These findings support the idea that the progressive accumulation of phospho-tau is associated with structural alterations of the GA including fragmentation and a decrease in the surface area and volume of GA elements. These alterations likely impact the processing and trafficking of proteins, which might contribute to neuronal dysfunction in AD.
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