Version 1
: Received: 22 October 2022 / Approved: 25 October 2022 / Online: 25 October 2022 (08:48:38 CEST)
Version 2
: Received: 3 December 2022 / Approved: 5 December 2022 / Online: 5 December 2022 (02:27:26 CET)
How to cite:
Gómez-Santos, D.J. Pioneering Organelle Structural Biology: Golgi Apparatus Dysfunction in Parkinson’s Disease, Neurodevelopmental Disorders, and Cancer. Preprints2022, 2022100383. https://doi.org/10.20944/preprints202210.0383.v1
Gómez-Santos, D.J. Pioneering Organelle Structural Biology: Golgi Apparatus Dysfunction in Parkinson’s Disease, Neurodevelopmental Disorders, and Cancer. Preprints 2022, 2022100383. https://doi.org/10.20944/preprints202210.0383.v1
Gómez-Santos, D.J. Pioneering Organelle Structural Biology: Golgi Apparatus Dysfunction in Parkinson’s Disease, Neurodevelopmental Disorders, and Cancer. Preprints2022, 2022100383. https://doi.org/10.20944/preprints202210.0383.v1
APA Style
Gómez-Santos, D.J. (2022). Pioneering Organelle Structural Biology: Golgi Apparatus Dysfunction in Parkinson’s Disease, Neurodevelopmental Disorders, and Cancer. Preprints. https://doi.org/10.20944/preprints202210.0383.v1
Chicago/Turabian Style
Gómez-Santos, D.J. 2022 "Pioneering Organelle Structural Biology: Golgi Apparatus Dysfunction in Parkinson’s Disease, Neurodevelopmental Disorders, and Cancer" Preprints. https://doi.org/10.20944/preprints202210.0383.v1
Abstract
The Golgi complex (GC) dysfunctions in Parkinson’s Disease (PD), neurodevelopmental disorders (NDDs), cancer, and organelle structural biology (OSB) can provide insights into therapeutic targets, gene therapy, and drug design. Primary defects and fragmentation within the GC are implicated in a wide range of neurodegenerative diseases. GC defects typically result in mislocation of proteins, accumulation of undegraded proteins, and impaired glycosylation of proteins. Inhibition of vesicular trafficking by α-synuclein (aSyn) may affect the dopamine-producing neurons and neuromodulators. GC regulates apoptosis during pathological mechanisms of neurological diseases and could provide new avenues in treatments through translation research. PD patients bearing the hereditary E46K disease mutation manifest the clinical picture of parkinsonism. How do we provide high resolution nanoimages of the GC during disease to capture dysfunction? Could we visualize the aSyn traffic jam between vesicles in the organelles ER and GC? OSB is emerging as a field as more technology advances and is more accessible. Structural studies of the GC will advance the field of neurological disease forward with an in depth understanding of dysfunction, fragmentation, and defects. Discoveries of the GC in PD, NDDs, and cancer would break new ground and provide translational medicine data of these diseases. Future research could be visualizing high angle annular dark field-STEM (HAADF-STEM) tomograms, cryogenic electron tomography (cryo-ET), multiplex correlative light and electron microscopy (cryo-CLEM), nanobody-assisted tissue immunostaining for volumetric EM (NATIVE) and using soft X-ray tomography (SXT) and computational reconstruction of the GC.
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
