CoChat
Sign Up
Cited by 626Alzheimer's disease research and treatmentsSphingolipid Metabolism and SignalingDementia and Cognitive Impairment Research

The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.

Substantial sulfatide deficiency and ceramide elevation in very early Alzheimer's disease: potential role in disease pathogenesis

Han, Xianlin, M. Holtzman, David, W. McKeel, Daniel, Kelley, John, Morris, John C.·2002·Journal of Neurochemistry
DOI 10.1046/j.1471-4159.2002.00997.x
Open this paper in CoChat — free account

Abstract

In addition to pathology in the gray matter, there are also abnormalities in the white matter in Alzheimer's disease (AD). Sulfatide species are a class of myelin‐specific sphingolipids and are involved in certain diseases of the central nervous system. To assess whether sulfatide content in gray and white matter in human subjects is associated with both the presence of Alzheimer's disease (AD) pathology as well as the stage of dementia, we analyzed the sulfatide content of brain tissue lipid extracts by electrospray ionization mass spectrometry from 22 subjects whose cognitive status at time of death varied from no dementia to very severe dementia. All subjects with dementia had AD pathology. The results demonstrate that: (i) sulfatides were depleted up to 93% in gray matter and up to 58% in white matter from all examined brain regions from AD subjects with very mild dementia, whereas all other major classes of lipid (except plasmalogen) in these subjects were not altered in comparison to those from age‐matched subjects with no dementia; (ii) there was no apparent deficiency in the biosynthesis of sulfatides in very mild AD subjects as characterized by the examination of galactocerebroside sulfotransferase activities in post‐mortem brain tissues; (iii) the content of ceramides (a class of potential degradation products of sulfatides) was elevated more than three‐fold in white matter and peaked at the stage of very mild dementia. The findings demonstrate that a marked decrease in sulfatides is associated with AD pathology even in subjects with very mild dementia and that these changes may be linked with early events in the pathological process of AD.

Overview

Integrity signals

Registry

Crossref · 10.1046/j.1471-4159.2002.00997.x

Cites

56 of 56 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Show all 56 references

Research works printed but not linked: 5

  1. 10.1139/y59-099 · DOI · Paper page
  2. 10.1042/bj3520079 · DOI
  3. Kolodny E. H., 1995, The Metabolic and Molecular Bases of Inherited Diseases, 2693
  4. Mattson M. P., 1997, Mother's legacy: mitochondrial DNA mutations and Alzheimer's disease, Trends Neurosci., 20, 373
  5. Suzuki K., 1995, The Metabolic and Molecular Bases of Inherited Diseases, 2671

Cited by

Sorted by citations

Items 401–500 of 625

Related

See all

Metadata

Authors
Han, X., M. Holtzman, D., W. McKeel, D., Kelley, J., & Morris, J. C.
Affiliations
Washington University in St. Louis (US)
Corresponding author
Han, Xianlin
ORCID
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2002-08
Volume
82
Issue
4
Pages
809-818
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
DOI
10.1046/j.1471-4159.2002.00997.x
OpenAlex
W1594975246
Cited by
626
References
56
Citations by year
2026: 24 · 2025: 26 · 2024: 29 · 2023: 32 · 2022: 32 · 2021: 29 · 2020: 32 · 2019: 22 · 2018: 29 · 2017: 33 · 2016: 34 · 2015: 24 · 2014: 33 · 2013: 33 · 2012: 36
FWCI
7.61
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 6 d)
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p41rr000954-34)
  • National Institute on Aging (P 50 AG05681, P50AG005681, P01 AG0 3991, P01AG003991)
  • National Center for Research Resources (P41RR00954-240043)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, sulfatide, ceramide, white matter, gray matter, brain lipid composition, pathogenesis
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Brain, Brain Chemistry, Ceramides, Dementia, Galactosylceramides, Humans, Neuropsychological Tests, Severity of Illness Index, Sphingomyelins, Sulfoglycosphingolipids, Sulfotransferases, Disease Progression, Spectrometry, Mass, Electrospray Ionization

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review