Cited by 383Complement system in diseasesAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Activation of the classical complement pathway in brain tissue of Alzheimer patients

McGeer, P.L., Akiyama, H., Itagaki, S., McGeer, E.G.·1989·Neuroscience Letters

Abstract

Positive immunohistochemical staining of Alzheimer brain tissue was obtained with antibodies to proteins associated with classical, but not the alternative, complement pathway. Clq, C3d, C4d are fractions of complement proteins that bind to tissue when the classical complement pathway is activated. Antibodies to these fractions stained senile plaques, dystrophic neurites and some neurofibrillary tangles. C5b-9 is the membrane attack complex which promotes cell lysis when assembled on the plasma membrane. An antibody to a neoantigenic site on this complex stained dystrophic neurites and many neurofibrillary tangles, but not extracellular amyloid. Properdin and fraction Bb of factor B, two proteins that bind to tissue when the alternative complement pathway is activated, were not detected immunohistochemically.

Integrity signals

Registry

Crossref · 10.1016/0304-3940(89)90843-4

Cites

15 of 15 references verified0 citation errors · 0 not checkable

Statistics

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

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?

  • In normal aging and tauopathy patients, C1q is dramatically upregulated and co-localizes with hyperphosphorylated tau, plaques, and neurofibrillary tangles in AD brain sections.

    “in normal aging [300] and in tauopathy patients [75], C1q is dramatically upregulated and is shown to co-localize with hyperphosphorylated tau, plaques and neurofibrillary tangles in AD brain sections [1, 219, 282]”
  • The classical complement cascade is triggered by C1q-complex.

    “The classical complement cascade is triggered by C1q-complex, and C1q is strongly expressed by microglia and enriched in the plaque cellular niche, as shown in Figure 4I and S4B (Eikelenboom et al. , 1988; McGeer et al. , 1989).”

    From Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease (2020) · cites this paper as McGeer et al., 1989

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
McGeer, P. L., Akiyama, H., Itagaki, S., & McGeer, E. G.
Affiliations
University of British Columbia (CA)
Corresponding author
McGeer, P.L.
Venue
Neuroscience Letters
Publisher
Elsevier BV
Published
1989-12
Volume
107
Issue
1-3
Pages
341-346
ISSN
0304-3940 (ISSN-L)
OpenAlex
W1980565738
Cited by
383
References
15
Citations by year
2025: 5 · 2024: 10 · 2023: 7 · 2022: 6 · 2021: 12 · 2020: 7 · 2019: 10 · 2018: 8 · 2017: 9 · 2016: 6 · 2015: 8 · 2014: 12 · 2013: 17 · 2012: 10
FWCI
3.94
Type
journal article
Language
en
Open access
closed
Locations
  • Neuroscience Letters (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
classical complement pathway, Alzheimer's disease, complement activation, C1q, C3d, C4d, C5b-9 membrane attack complex, amyloid plaques, dystrophic neurites, neurofibrillary tangles, amyloid, alternative complement pathway, properdin, factor B
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Brain, Inclusion Bodies, Complement Activation, Complement Pathway, Classical, Complement C4, Humans, Immunohistochemistry, Neurofibrils, Peptide Fragments, Complement C1q, Complement C3d, Complement C4b, Complement Membrane Attack Complex

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