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2000
Volume 14, Issue 6
  • ISSN: 1567-2050
  • E-ISSN: 1875-5828

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.

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/content/journals/car/10.2174/1567205014666170117094038
2017-06-01
2025-04-22
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/content/journals/car/10.2174/1567205014666170117094038
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  • Article Type:
    Research Article
Keyword(s): Alzheimer's disease; Chol-1α antigen; cholinergic neuron; dementia; ganglioside
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