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PrP antibodies do not trigger mouse hippocampal neuron apoptosis
Peter-Christian Klöhn1, Michael Farmer, Jacqueline M Linehan
1Medical Research Council (MRC) Prion Unit and Department of Neurodegenerative Disease, University College London Institute of Neurology, Queen Square, London WC1N 3BG, UK.
Science (New York, N.Y.)
|January 7, 2012
Summary
Monoclonal antibodies targeting prion protein (PrP) show therapeutic potential for prion and Alzheimer's diseases. Extensive studies found no evidence of apoptosis, challenging a key model of prion neurotoxicity.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Monoclonal antibodies (mAbs) against prion protein (PrP) like ICSM18 and 35 delay prion disease in mice.
- Humanized versions are investigated as therapeutics for prion and Alzheimer's diseases.
- Previous studies reported apoptosis following intracerebral anti-PrP mAb injection, proposing a neurotoxicity model.
Purpose of the Study:
- To investigate the potential for apoptosis induced by anti-PrP mAbs.
- To evaluate the validity of the prion neurotoxicity model based on PrP cross-linking.
Main Methods:
- Administration of anti-PrP mAbs (ICSM18, 35, humanized ICSM18) and previously reported proapoptotic antibodies.
- Extensive studies to assess for evidence of apoptosis.
Main Results:
- No evidence of apoptosis was observed in response to anti-PrP mAb administration.
- The findings question the proposed mechanism of prion neurotoxicity via PrP cross-linking.
Conclusions:
- Anti-PrP monoclonal antibodies do not induce apoptosis.
- The influential model of prion neurotoxicity via cross-linking of cell surface PrP is challenged by these findings.
