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
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.