Evidence map›Paper›PMID 24495408›Full record

ReviewAlzheimer's research & therapy2014

Fyn kinase inhibition as a novel therapy for Alzheimer's disease.

Haakon B Nygaard, Christopher H van Dyck, Stephen M Strittmatter

Open access · goldAbstract readReview
In one paragraph

Review in Alzheimer's research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 197 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. The Src-Family Kinases Hck, Fgr and Lyn Drive Immune Complex-Mediated Glomerulonephritis Through the Syk Tyrosine Kinase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Article
  6. Article
  7. Protein kinases as therapeutic targets in Alzheimer's disease: challenges, insights, and new frontiers.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  8. Article
  9. Identification of Novel Kv1.3 Channel-Interacting Proteins Using Proximity Labelling in T-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

49 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Haakon B NygaardDepartment of Neurology, Yale University School of Medicine, PO Box 208018, New Haven, CT 06520, USA ; Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, 295 Congress Avenue, BCMM 436, New Haven, CT 06536, USA.
Christopher H van DyckAlzheimer's Disease Research Unit, Yale University School of Medicine, 1 Church Street, Suite 600, New Haven, CT 06510, USA ; Department of Psychiatry, Yale University School of Medicine, 300 George Street, Suite 901, New Haven, CT 06511, USA.
Stephen M StrittmatterDepartment of Neurology, Yale University School of Medicine, PO Box 208018, New Haven, CT 06520, USA ; Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, 295 Congress Avenue, BCMM 436, New Haven, CT 06536, USA.
Yale University · US

Funding

Prion Protein in Alzheimer's Disease PathophysiologyR01AG034924 · NIA · YALE UNIVERSITY · PI STEPHEN M STRITTMATTER · 2010 to 2026
$9.6M
Fyn Inhibition by AZD0530 for Alzheimers DiseaseUH3TR000967 · NCATS · YALE UNIVERSITY · PI NYGAARD, HAAKON BERGE, STRITTMATTER, STEPHEN M · 2014 to 2016
$8.5M
NCATS NIH HHS UH3 TR000967NIA NIH HHS R01 AG034924
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disorder, afflicting more than one-third of people over the age of 85. While many therapies for AD are in late-stage clinical testing, rational drug design based on distinct signaling pathways in this disorder is only now emerging. Here we review the putative signaling pathway of amyloid-beta (Aβ), by which the tyrosine kinase Fyn is activated via cell surface binding of Aβ oligomers to cellular prion protein. Several lines of evidence implicate Fyn in the pathogenesis of AD, and its interaction with both Aβ and Tau renders Fyn a unique therapeutic target that addresses both of the major pathologic hallmarks of AD. We are currently enrolling patients in a phase Ib study of saracatinib (AZD0530), a small molecule inhibitor with high potency for Src and Fyn, for the treatment of AD. The results of this trial and a planned phase IIa multisite study will provide important data regarding the potential for this therapeutic strategy in AD.

Identifiers

PMID24495408
PMCPMC3978417
OpenAlexW2110979697

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.