Ganglioside catabolism is altered in fibroblasts and leukocytes from Alzheimer's disease patients

Kalanj-Bognar, Svjetlana

doi:10.1016/j.neurobiolaging.2005.06.012

Cited by 5 publications

(3 citation statements)

References 25 publications

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“…During aging and neurodegeneration, the physicochemical properties of membranes are altered. This can result in imbalances in the proportion of lipids in membranes and/or changed ratios of membrane lipids, which may contribute to the pathogenesis of AD (22). In brain cells, ganglioside and lipid abnormalities, in addition to pathogenic Ab production, may contribute to the pathological conditions found in AD (20).…”

Section: Ganglioside Metabolism In Admentioning

confidence: 99%

Thematic Review Series: Sphingolipids. Role of ganglioside metabolism in the pathogenesis of Alzheimer's disease—a review

Ariga

McDonald

2008

Journal of Lipid Research

290

236

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Section: Ganglioside Metabolism In Admentioning

confidence: 99%

Thematic Review Series: Sphingolipids. Role of ganglioside metabolism in the pathogenesis of Alzheimer's disease—a review

Ariga

McDonald

2008

Journal of Lipid Research

290

236

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“…1,2 Gangliosides are acidic glycosphingolipids of the plasma membranes which are mainly present in neural membranes (especially in presynaptic membranes). In addition to their role as surface markers in the outer leaflet of cell membranes, gangliosides are thought to have multiple biological functions.…”

Section: Introductionmentioning

confidence: 99%

“…Lipids play a potential role in the pathology of many neurodegenerative disorders of central nervous system like dementia and Alzheimer’s disease (AD). 1,2…”

Section: Introductionmentioning

confidence: 99%

Antibodies Against Gangliosides in Patients With Dementia

Hatzifilippou

Koutsouraki

Costa

et al. 2014

Am J Alzheimers Dis Other Demen

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SV2 frustrating exocytosis at the semi‐diffusor synapse

Vautrin

2009

Synapse

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Presynaptic exocytosis is the mechanism commonly believed to release transmitters by diffusion through a pore opening during vesicular membrane fusion with the plasmalemma, but evidence suggesting that exocytosis and transmitter release are two separate steps of synaptic transmission is accumulating. Vesicular glycoconjugates such as Synaptic Vesicle Protein 2 (SV2) proteoglycans and gangliosides retain transmitters in a nondiffusible form and are transported to the synaptic cleft where they contribute forming a dense synaptomatrix. Transmitters are permanently present in synaptic clefts and readily releasable transmitter is easily accessible from the outer side of the presynaptic membrane suggesting that synaptomatrix glycoconjugates prevent immediate release after PKC-dependent exocytosis. The calcium sensor synaptotagmin is also present at the presynaptic plasma membrane and binds SV2 suggesting a direct coupling between the calcium transient and transmitter release from the synaptomatrix. A quantitative coupling of the cytosolic calcic transient to transmitter release from the synaptomatrix explains better complexity and plasticity of miniature postsynaptic signals hitherto difficult to account for in exocytic terms. This alternative representation of synaptic transmission in which the same components of the synaptomatrix support adhesion and signaling functions may cast new lights on synaptic diseases such as Alzheimer's disease.

show abstract

Ganglioside catabolism is altered in fibroblasts and leukocytes from Alzheimer's disease patients

Cited by 5 publications

References 25 publications

Thematic Review Series: Sphingolipids. Role of ganglioside metabolism in the pathogenesis of Alzheimer's disease—a review

Thematic Review Series: Sphingolipids. Role of ganglioside metabolism in the pathogenesis of Alzheimer's disease—a review

Antibodies Against Gangliosides in Patients With Dementia

SV2 frustrating exocytosis at the semi‐diffusor synapse

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