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Updated: Aug 7, 2026

Assaying β-amyloid Toxicity using a Transgenic C. elegans Model
Published on: October 10, 2010
Transforming growth factor beta2 autocrinally mediates neuronal cell death induced by amyloid-beta
Yuichi Hashimoto1, Mikiro Nawa, Tomohiro Chiba
1Department of Pharmacology, KEIO University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Abstract:
Amyloid beta (Abeta), the major component of the senile plaques of Alzheimer's disease, is implicated in neuronal cell death. We have found that Abeta42, a neurotoxic form of Abeta peptide, induces both neuronal and glial expression of TGFbeta2. We have further demonstrated that the addition into culture media of neutralizing antibody to TGFbeta2 or a large amount of the recombinant soluble amyloid precursor protein alpha, the extracellular domain of amyloid precursor protein (APP) generated by alpha secretase, suppresses death in primary cortical neurons (PCNs) induced by Abeta42 in vitro. Combined with the finding in our recent study indicating that TGFbeta2 is a neuronal cell death-inducing ligand for APP, it is suggested that TGFbeta2 is an autocrinal mediator for Abeta42-induced death in PCNs.
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