Fragmentation of the Golgi complex of
dopaminergic neurons in human substantia nigra: New cytopathological findings in Parkinson's disease
Mónica Tomás1*, Emma Martínez-Alonso2, Narcisa Martínez-Martínez2, Mireia Cara-Esteban1 and José A. Martínez-Menárguez2*
1Department of Human Anatomy and Embryology, Medical School, University of Valencia, Valencia and 2Department of Cell Biology and Histology, Medical School, University of Murcia, Murcia, Spain
*Both authors contributed equally as co-princpal authors
Corresponding Author: Prof. Dr. José A. Martínez-Menárguez, Department of Cell Biology and Histology, Medical School, University of Murcia, 30100 Murcia, Spain. e-mail: jamartin@um.es or Prof. Dr. Mónica Tomás, Department of Human Anatomy and Embriology, University of Valencia, 46010 Valencia, Spain. e-mail: monica.tomas@uv.es
Summary. Fragmentation of the Golgi ribbon is a common feature of Parkinson's disease and other neurodegenerative diseases. This alteration could be the consequence of the anterograde and retrograde transport imbalance, α-synuclein aggregates, and/or cytoskeleton alterations. Most information on this process has been obtained from cellular and animal experimental models, and as such, there is little information available on human tissue. If the information on human tissue was available, it may help to understand the cytopathological mechanisms of this disease. In the present study, we analyzed the morphological characteristics of the Golgi complex of dopaminergic neurons in human samples of substantia nigra of control and Parkinson's disease patients. We measured the expression levels of putative molecules involved in Golgi fragmentation, including α-synuclein, tubulin, and Golgi-associated regulatory and structural proteins. We show that, as a consequence of the disease, the Golgi complex is fragmented into small stacks without vesiculation. We found that only a limited number of regulatory proteins are altered. Rab1, a small GTPase regulating endoplasmic reticulum-to-Golgi transport, is the most dramatically affected, being highly overexpressed in the surviving neurons. We found that the SNARE protein syntaxin 5 forms extracellular aggregates resembling the amyloid plaques characteristic of Alzheimer's disease. These findings may help to understand the cytopathology of Parkinson's disease. Histol Histopathol 36, 47-60 (2021)
Key words: Golgi complex, Parkinson's disease, Dopaminergic neurons, Substantia nigra, Membrane traffic, α-synuclein
DOI: 10.14670/HH-18-270
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©The Author(s) 2021. Open Access. This article is licensed under a Creative Commons CC-BY International License. |
