Brain Gangliosides in Alzheimer’s Disease: Increased Expression of Cholinergic Neuron-Specific Gangliosides

Title:Brain Gangliosides in Alzheimer’s Disease: Increased Expression of Cholinergic Neuron-Specific Gangliosides

Volume: 14 Issue: 6

Author(s): Yuki Fukami, Toshio Ariga, Mitsunori Yamada and Nobuhiro Yuki*

Affiliation:

• Departments of Medicine and Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Unit 09-01, Centre for Translational Medicine, 14 Medical Drive,Singapore

Keywords: Alzheimer's disease, Chol-1α antigen, cholinergic neuron, ganglioside, dementia.

Abstract: Background: Gangliosides are enriched in the neuronal membranes. Gangliosides are shown to interact with amyloid-β proteins, leading to formation of amyloid fibrils in Alzheimer’s disease (AD) brains. Several earlier studies indicated that the alterations of ganglioside metabolism could contribute the pathogenesis of AD.

Methods: Gangliosides were isolated from the frontal lobes in five patients with AD and three control subjects. Gangliosides were assessed by high performance thin-layer chromatography (HPTLC) with resorcinol staining and immunostaining using mouse monoclonal antibodies against cholinergic neuronspecific (Chol-1α) gangliosides.

Results: In all AD brains, not only the total sialic acid content but also a-series gangliosides, GM1 and GD1a, were dramatically reduced as compared with those in control subjects. These results are a hallmark of the pathogenesis in AD. In contrast, Chol-1α gangliosides, GT1aα and GQ1bα, which are specific markers of cholinergic neurons, were significantly increased in AD brains.

Conclusion: The expression of Chol-1α gangliosides may be caused by a compensation to preserve the function of the cholinergic neuron and play an important role in cholinergic synaptic transmission.

Cite this article as:

Fukami Yuki, Ariga Toshio, Yamada Mitsunori and Yuki Nobuhiro*, Brain Gangliosides in Alzheimer’s Disease: Increased Expression of Cholinergic Neuron-Specific Gangliosides, Current Alzheimer Research 2017; 14 (6) . https://dx.doi.org/10.2174/1567205014666170117094038

DOI https://dx.doi.org/10.2174/1567205014666170117094038	Print ISSN 1567-2050
Publisher Name Bentham Science Publisher	Online ISSN 1875-5828