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. 2017;14(6):586-591.
doi: 10.2174/1567205014666170117094038.

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

Affiliations

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

Yuki Fukami et al. Curr Alzheimer Res. 2017.

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.

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

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