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Volume 8 Journal of Alzheimers Disease & Parkinsonism
ISSN: 2161-0460 Euro Dementia 2018
May 24-25, 2018
May 24-25, 2018 | Vienna, Austria
11th International Conference on
Alzheimers Disease & Dementia
The role of N-acetylglucosaminyltransferase III in Alzheimer’s disease progression
Ying Wang, Song Chen and Xiangdong Gao
China Pharmaceutical University, China
The pathogenic mechanism of Alzheimer’s disease (AD) has not been clearly defined, and many factors have been
discovered to explain this multifactorial disorder. The alteration of glycoprotein glycans in AD has been highlighted
recently. It has been reported that the bisecting N-acetylglucosamine (GlcNAc) levels were higher in the cerebrospinal fluid
of most AD patients, which indicates that N-acetylglucosaminyltransferase III (GnT-III), a glycosyltransferase responsible
for synthesizing a bisecting GlcNAc residue, may play an important role in the development of AD. In our previous studies,
we demonstrated that the levels of GnT-III and bisecting GlcNAc were increased in AD models, and glucagon-like peptide-1
(GLP-1) receptor agonists could downregulate aberrant expression of GnT-III through the Akt/GSK-3β/β-catenin signaling
pathway in neurons. Here, we further explored the role of GnT-III in AD progression. We overexpressed GnT-III in PC12
cells and found that the intracellular reactive oxygen species (ROS) was increased significantly in GnT-III overexpressing
cells. The mitochondrial structure was damaged and the mitochondrial membrane potential (Δψm) tested by JC-1 probe was
lower in GnT-III overexpressing cells, which indicated that the mitochondrial function might be damaged by aberrant GnT-III
expression. Besides, we also tested the GLP-1 receptor signaling mediated by GLP-1 and found that overexpression of GnT-III
disrupted the normal GLP-1 receptor signaling in neurons. In conclusion, our findings reveal that GnT-III could be a potential
therapeutic target for AD.
Recent Publications
1. Wang Y, Chen S, Xu Z, Chen S T, YaoWB, et al. (2018) GLP-1 receptor agonists downregulate aberrant GnT-III expression
in Alzheimer's disease models through the Akt/GSK-3β/β-catenin signaling. Neuropharmacology 131:190–199.
2. Chen S, Yin L, Xu Z, An F M, Liu A R, et al. (2016) Inhibiting receptor for advanced glycation end product (AGE) and
oxidative stress involved in the protective effect mediated by glucagon-like peptide-1 receptor on AGE induced neuronal
apoptosis. Neurosci Lett. 612:193–198.
3. An F M, Chen S, Xu Z, Yin L, Wang Y, et al. (2015) Glucagon-like peptide-1 regulates mitochondrial biogenesis and
tau phosphorylation against advanced glycation end product-induced neuronal insult: Studies in vivo and in vitro.
Neuroscience 300:75–84.
Biograpy
Ying Wang is a PhD student of Microbiology and Biochemical Pharmacy at the China Pharmaceutical University. She is investigating the molecular pathogenesis of
Alzheimer’s disease, especially about the relationship between protein glycosylation and Alzheimer’s disease.
Ying Wang et al., J Alzheimers Dis Parkinsonism 2018, Volume 8
DOI:10.4172/2161-0460-C3-042