Golgi dysfunction in Alzheimer disease: from human multiomic signatures to therapeutic targets
- 1Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea
- 2Convergence Dementia Research Center, Medical Research Center, Seoul National University, Seoul, Republic of Korea
Abstract
Deciphering the intricate pathogenesis of Alzheimer disease (AD) has been a highly demanding task for researchers for decades. Evidence from from human multiomic studies provides critical insights into complex disease mechanisms and drives novel findings. However, the data are often selectively comprehended, leaving a few notable factors underappreciated in the research field. We focus on the Golgi apparatus, one of the most undervalued organelles in AD research, to demonstrate its multidimensional contribution to the pathogenesis. Given the importance of Golgi in modulating intracellular protein and lipid homeostasis, implication of Golgi in AD pathogenesis deserves thorough investigation. In this review, we describe changes in Golgi morphology and function in AD, and summarize specific Golgi-related factors discovered by genomic, transcriptomic, proteomic, and lipidomic data using human samples. Based on the findings, we demonstrate mechanistic link of Golgi-related factors to AD pathogenesis and highlight potential therapeutic strategies to modify Golgi-mediated pathogenesis. Overall, Golgi dysfunction may serve as a notable mechanistic hub of AD pathogenesis, making it a promising target for development of novel therapeutic strategies.
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BibTeX
@article{song2026golgi,
title = {{Golgi dysfunction in Alzheimer disease: from human multiomic signatures to therapeutic targets}},
author = {Jaehoon Song and Seung-Jae Lee and Inhee Mook-Jung},
journal = {Experimental and Molecular Medicine},
year = {2026},
month = oct,
doi = {10.1038/s12276-026-01851-8},
url = {https://doi.org/10.1038/s12276-026-01851-8},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Golgi dysfunction in Alzheimer disease: from human multiomic signatures to therapeutic targets
AU - Jaehoon Song
AU - Seung-Jae Lee
AU - Inhee Mook-Jung
PY - 2026
DA - 2026/10/01
JO - Experimental and Molecular Medicine
DO - 10.1038/s12276-026-01851-8
UR - https://doi.org/10.1038/s12276-026-01851-8
AB - Deciphering the intricate pathogenesis of Alzheimer disease (AD) has been a highly demanding task for researchers for decades. Evidence from from human multiomic studies provides critical insights into complex disease mechanisms and drives novel findings. However, the data are often selectively comprehended, leaving a few notable factors underappreciated in the research field. We focus on the Golgi apparatus, one of the most undervalued organelles in AD research, to demonstrate its multidimensional contribution to the pathogenesis. Given the importance of Golgi in modulating intracellular protein and lipid homeostasis, implication of Golgi in AD pathogenesis deserves thorough investigation. In this review, we describe changes in Golgi morphology and function in AD, and summarize specific Golgi-related factors discovered by genomic, transcriptomic, proteomic, and lipidomic data using human samples. Based on the findings, we demonstrate mechanistic link of Golgi-related factors to AD pathogenesis and highlight potential therapeutic strategies to modify Golgi-mediated pathogenesis. Overall, Golgi dysfunction may serve as a notable mechanistic hub of AD pathogenesis, making it a promising target for development of novel therapeutic strategies.
SN - 2092-6413
SN - 1226-3613
ER -