Ganglioside monoclonal antibody (A2B5) labels Alzheimer's neurofibrillary tangles

Emory, Carolyn; Thomas, Alan W.; Frey, William H.

doi:10.1212/wnl.37.5.768

Cited by 49 publications

(15 citation statements)

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“…X-ray microprobe analysis of these intact prcPHF confirmed that they were nonproteinaceous in composition [19]. An independent laboratory has previously shown that neurofibrillary tangles could be immunolabeled in situ with a monoclonal antibody to a ganglioside [20]. They have since shown by immunoelectron microscopy that this antibody will immunolabel isolated, intact PHF [21].…”

Section: Introductionmentioning

confidence: 76%

Analysis of the core components of Alzheimer paired helical filaments A gas chromatography/mass spectrometry characterization of fatty acids, carbohydrates and long‐chain bases

1995

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We have carried out a fatty acid and carbohydrate compositional analysis of the protease-resistant core of paired helical filaments (prcPHF) isolated from six Alzheimer's diseased brains. Fatty acids, long-chain bases and monosaccharides were characterized by gas chromatography/mass spectrometry (GC/ MS) of fatty acid methyl esters, trimethylsilylated long-chain bases, peraeetylated alditol acetates and trimethylsilyl methyl glycosides. Glucose and mannose were found to be the only carbohydrate components. Four of the six prcPHF samples contained only glucose while the remaining two samples contained between 30--40% mannose in addition to glucose. None of the samples were found to contain either hydroxylated fatty acids or long-chain bases. The average fatty acid profile of prcPHF was highest in stearic (C18:0) and palmitic acids (C16:0) with less than 10% unsaturated fatty acids. By comparing the carbohydrate and lipid composition of prcPHF to similar data for other brain glycolipids, it was determined that prcPHF is a unique glycolipid, distinct from cerebrosides, gangliosides or brain phospbolipids. The fatty acid and carbohydrate composition of a glycolipid isolated from a population of normal brains according to the prcPHF protocol was found be identical to that of prcPHF glycolipid. It is possible that subtle differences in structure or indigenous factors are responsible for the initiation of PHF formation in vivo.

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Section: Introductionmentioning

confidence: 76%

Analysis of the core components of Alzheimer paired helical filaments A gas chromatography/mass spectrometry characterization of fatty acids, carbohydrates and long‐chain bases

1995

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“…It is worthy to note that an aberrant expression of A2B5-positive gangliosides was observed in neurofibrillary tangles and dystrophic neurites in Alzheimer's disease brain [24,25] and that GD3 was highly enriched in the plaques of multiple sclerosis [26,27[. The elucidation of ganglioside marker in fetal human brain cell cultures might help us to better under stand the alterations in ganglioside biosynthesis in the human CNS disorders.…”

Section: Introductionmentioning

confidence: 99%

Ganglioside Markers GD3, GD2, and A2B5 in Fetal Human Neurons and Glial Cells in Culture

Satoh¹,

Kim²

1995

Dev Neurosci

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Expression of ganglioside markers GD3, GD2, and A2B5 was investigated in primary cell cultures isolated from fetal human brains of 12–15 weeks gestation by immunocytochemistry. None of neuron-specific enolase (NSE)⁺ neurons expressed GD3, while large numbers of NSE⁺ neurons expressed GD2 (72%) or A2B5 (48%). In GFAP⁺ astrocytes, GD3 was expressed in a small population (3%) with a high proliferative capacity. GD2 expression was observed in 20% of GFAP⁺ astrocytes, while A2B5 was identified in a very small number (2%) of GFAP⁺ astrocytes. GD2 was coexpressed in a small population (11%) of GD3⁺ astrocytes, while A2B5 was colocalized in more than 50% of GD3⁺ astrocytes. In galactocerebroside⁺ oligodendrocytes, GD3 expression was not observed but a small population (8–9%) expressed GD2 and A2B5, In Ricinus communis agglutinin (RCA)⁺ microglia, neither GD3, GD2, nor A2B5 were identified. Our results indicate that in fetal human brain cell cultures, GD3 is expressed in a small population of astrocytes, while both GD2 and A2B5 are expressed in a large population of neurons and smaller populations of astrocytes and oligodendrocytes. Our results suggest that both GD3 and A2B5, cell type-specific markers for oligodendrocyte-type 2 astrocyte progenitor cells in the rat central nervous system, could not be utilized as valid markers for glial precursor cells in fetal human brain cell cultures.

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“…Regarding this, a variety of neurodegenerative disorders are associated with an increase in the amount of gangliosides in the cerebrospinal fluid [3][4][5]. And also, gangliosides have been localized to neurofibrillary tangles in brain tissue from AD patients, and Betz cells of the precentral gyrus in amyotrophic lateral sclerosis (ALS) patients [6][7][8]. Especially, GD1a was detected in dystrophic neurons and accumulated in some senile plaques, suggesting the contribution of senile plaques formation in AD brains [9].…”

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confidence: 99%

Disialogangliosides induce neurodegeneration in rat mesencephalic cultures

Chung

Jin

2006

Biochemical and Biophysical Research Communications

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Ganglioside monoclonal antibody (A2B5) labels Alzheimer's neurofibrillary tangles

Cited by 49 publications

References 0 publications

Analysis of the core components of Alzheimer paired helical filaments A gas chromatography/mass spectrometry characterization of fatty acids, carbohydrates and long‐chain bases

Analysis of the core components of Alzheimer paired helical filaments A gas chromatography/mass spectrometry characterization of fatty acids, carbohydrates and long‐chain bases

Ganglioside Markers GD3, GD2, and A2B5 in Fetal Human Neurons and Glial Cells in Culture

Disialogangliosides induce neurodegeneration in rat mesencephalic cultures

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