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Letters to Editor
Nature Medicine 7, 977 - 978 (2001)
doi:10.1038/nm0901-977
Inhibition of post-ischemic brain injury by clusterin overexpression
Philippe Wehrli1, Yves Charnay2, Philippe Vallet2, Guang Zhu4, Judith Harmony4, Bruce Aronow4, Jürg Tschopp5, Constantin Bouras2, Isabelle Viard-Leveugle1, Lars E. French1 & Panteleimon Giannakopoulos3
- Department of Dermatology, Geneva University Medical School, Geneva, Switzerland
- Division of Neuropsychiatry, Department of Psychiatry University of Geneva School of Medicine, Geneva, Switzerland
- Clinic of Geriatric Psychiatry, Department of Psychiatry University of Geneva School of Medicine, Geneva, Switzerland
- Division of Molecular Developmental Biology Children's Hospital Research Foundation Cincinnati, Ohio, USA
- Institute of Biochemistry, Lausanne University Lausanne, Switzerland
e-mail: giannako@cmu.unige.ch
Previous reports have suggested that clusterin might protect against apoptotic cell death and neurodegeneration1, 2. In disagreement with these data, Han et al.3 recently reported in the March issue of Nature Medicine that clusterin contributes to caspase-3–independent brain injury following neonatal hypoxia-ischemia in a gene-dose–dependent manner.
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