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© Marion Coolen
Radial glia neural stem cells of the adult zebrafish telencephalon electroporated with a membrane tagged GFP
Publication : EMBO reports

A gamma-secretase inhibitor blocks Notch signaling in vivo and causes a severe neurogenic phenotype in zebrafish

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in EMBO reports - 01 Jul 2002

Geling A, Steiner H, Willem M, Bally-Cuif L, Haass C

Link to Pubmed [PMID] – 12101103

EMBO Rep. 2002 Jul;3(7):688-94

Inhibition of amyloid beta-peptide (Abeta) production by blocking gamma-secretase activity is at present one of the most promising therapeutic strategies to slow progression of Alzheimer’s disease pathology. gamma-secretase inhibitors apparently block Abeta generation via interference with presenilin (PS) function. Besides being an essential component of the gamma-secretase complex, PS itself may be an aspartyl protease with gamma-secretase activity, which is not only required for Abeta production but also for a similar proteolytic process involved in Notch signaling. Here we demonstrate that treatment of zebrafish embryos with a known gamma-secretase inhibitor affects embryonic development in a manner indistinguishable from Notch signaling deficiencies at morphological, molecular and biochemical levels. This indicates severe side-effects of gamma-secretase inhibitors in any Notch-dependent cell fate decision and demonstrates that the zebrafish is an ideal vertebrate system to validate compounds that selectively affect Abeta production, but not Notch signaling, under in vivo conditions.

http://www.ncbi.nlm.nih.gov/pubmed/12101103