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Cited by 101Alzheimer's disease research and treatmentsSphingolipid Metabolism and SignalingLipid metabolism and biosynthesis

Potential mechanisms contributing to sulfatide depletion at the earliest clinically recognizable stage of Alzheimer’s disease: a tale of shotgun lipidomics

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Han, Xianlin·2007·Journal of Neurochemistry
DOI 10.1111/j.1471-4159.2007.04708.xPMC PMC2147059
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Abstract

Shotgun lipidomics is a rapidly developing technology, which identifies and quantifies individual lipid molecular species directly from lipid extracts of biological samples. Alterations in lipid molecular species in the brain induced by neurodegenerative diseases, such as Alzheimer’s disease (AD) could provide fundamental clues to disease pathogenesis. To date, the cause(s) leading to AD pathogenesis are still unknown and apolipoprotein E (apoE) allele 4 is the only known major risk factor for this devastating disease. By utilizing shotgun lipidomics, we have recently shown that a substantial and specific depletion of sulfatide (a class of specialized myelin sphingolipids) is present in postmortem brains from subjects at the earliest clinically recognizable stage of AD. In subsequent studies to identify the biochemical mechanisms underlying sulfatide depletion at this very mild stage of AD, we have found that apoE is associated with sulfatide transport and mediates sulfatide homeostasis in the nervous system through lipoprotein metabolism pathways and that alterations in apoE‐mediated sulfatide trafficking can lead to sulfatide depletion in the brain. Thus, a working model related to the potential biochemical mechanisms underlying sulfatide depletion in AD can be derived based on these results. Collectively, the results obtained from lipidomic analyses of brain samples provide important insights into the biochemical mechanisms underlying AD pathogenesis.

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  • Multiple myelin-enriched lipid classes (such as galactosylceramides, sulfatides, and plasmalogens) are increasingly recognized as vulnerable nodes in AD.

    “multiple myelin-enriched lipid classes (such as galactosylceramides, sulfatides, and plasmalogens) are increasingly recognized as vulnerable nodes in AD [42, 43].”

    From PLCγ2 deficiency compromises systemic immune tolerance and erodes myelin homeostasis while enhancing oxidative metabolism in the mouse brain (2026) · cites this paper as [42]

    The paper reports substantial sulfatide depletion in very mild AD and identifies pGPEtn (a plasmalogen lipid) as another class with altered content (Abstract; page unavailable). But it reports no significant change in cerebrosides, which include galactosylceramides. It therefore does not support the claim for all three listed classes. (LLM, conf=0.88)

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Sorted by citations

Authors
Han, X.
Affiliations
Washington University in St. Louis (US)
Corresponding author
Han, Xianlin
ORCID
Han, Xianlin
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2007-11
Volume
103
Issue
s1
Pages
171-179
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
DOI
10.1111/j.1471-4159.2007.04708.x
PMC
PMC2147059
OpenAlex
W2024289001
Cited by
101
References
4
Citations by year
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FWCI
0.71
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 5 d)
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Aging (R01 AG23168, R01AG023168)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
Alzheimer's disease, apolipoprotein E, APOE ε4, lipoprotein metabolism, postmortem brain, pathogenesis, lipidomics
MeSH terms
Alzheimer Disease, Animals, Humans, Sulfoglycosphingolipids, Lipid Metabolism

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