Specificity and potential mechanism of sulfatide deficiency in Alzheimer's disease

an electrospray ionization mass spectrometric study.

H. Cheng, J. Xu, D. W. McKeel, Xianlin Han

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

Recently, we have demonstrated that sulfatide content was substantially depleted in post-mortem brain samples from subjects with very mild Alzheimer's disease (AD) relative to age-matched controls. However, it is unknown if the observed sulfatide deficiency is AD-specific and what mechanism(s) lead to this depletion. By exploiting the advantages of electrospray ionization mass spectrometry techniques, we examined the specificity and a potential mechanism of sulfatide deficiency in AD in the study. In contrast to the sulfatide depletion observed in AD, it was found that the sulfatide content in post-mortem brain samples from subjects with Parkinson's disease and dementia with Lewy bodies was either higher than or comparable to that observed from controls, respectively, suggesting that sulfatide deficiency is likely specific to AD. Examination of lipid alterations in cultured embryonic rat brain oligodendrocytes treated with amyloid-beta peptide demonstrated that there was no alteration in sulfatide content up to a 24-hr interval after amyloid-beta addition/treatment. However, there were significant decreases in plasmenylethanolamine and increases in sphingomyelin content in the same study. These findings suggest that sulfatide deficiency in AD is unlikely mediated directly by amyloid-beta peptide accumulation. Thus, these results illustrate the specificity of sulfatide deficiency in AD and exclude amyloid-beta accumulation as a factor directly contributing to sulfatide deficiency in AD.

Original languageEnglish (US)
Pages (from-to)809-818
Number of pages10
JournalCellular and molecular biology (Noisy-le-Grand, France)
Volume49
Issue number5
StatePublished - Jul 1 2003
Externally publishedYes

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Sulfoglycosphingolipids
Electrospray ionization
Alzheimer Disease
Brain
Amyloid beta-Peptides
Amyloid
Lewy Body Disease
Sphingomyelins
Electrospray Ionization Mass Spectrometry
Oligodendroglia
Mass spectrometry
Parkinson Disease
Rats

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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abstract = "Recently, we have demonstrated that sulfatide content was substantially depleted in post-mortem brain samples from subjects with very mild Alzheimer's disease (AD) relative to age-matched controls. However, it is unknown if the observed sulfatide deficiency is AD-specific and what mechanism(s) lead to this depletion. By exploiting the advantages of electrospray ionization mass spectrometry techniques, we examined the specificity and a potential mechanism of sulfatide deficiency in AD in the study. In contrast to the sulfatide depletion observed in AD, it was found that the sulfatide content in post-mortem brain samples from subjects with Parkinson's disease and dementia with Lewy bodies was either higher than or comparable to that observed from controls, respectively, suggesting that sulfatide deficiency is likely specific to AD. Examination of lipid alterations in cultured embryonic rat brain oligodendrocytes treated with amyloid-beta peptide demonstrated that there was no alteration in sulfatide content up to a 24-hr interval after amyloid-beta addition/treatment. However, there were significant decreases in plasmenylethanolamine and increases in sphingomyelin content in the same study. These findings suggest that sulfatide deficiency in AD is unlikely mediated directly by amyloid-beta peptide accumulation. Thus, these results illustrate the specificity of sulfatide deficiency in AD and exclude amyloid-beta accumulation as a factor directly contributing to sulfatide deficiency in AD.",
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