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p25 protein in neurodegeneration

Author

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  • Byong Chul Yoo

    (University of Vienna)

  • Gert Lubec

    (University of Vienna)

Abstract

The normal development of the mammalian central nervous system requires a protein kinase known as Cdk5, the activity of which depends on its interaction with a regulatory subunit, p35. An abnormal truncated form of p35 (p25) produced by the action of proteases1,2 can also activate Cdk5, but causes apoptotic cell death in cultured primary neurons3. Patrick et al. have reported that p25 accumulates 20–40-fold in brain lysates from patients with Alzheimer's disease, and infer that p25 may contribute to the pathogenesis of neurodegeneration3. Here we show that the amount of p25 in the frontal cortex of patients with Alzheimer's disease or Down's syndrome is actually lower than in controls. Although there is evidence for a role for p25 in neurodegeneration from cells in culture2,3 and in rats4 and mice5, our contradictory finding casts doubt on the involvement of p25 in neurodegenerative conditions such as Alzheimer's disease and Down's syndrome.

Suggested Citation

  • Byong Chul Yoo & Gert Lubec, 2001. "p25 protein in neurodegeneration," Nature, Nature, vol. 411(6839), pages 763-764, June.
    • Handle: RePEc:nat:nature:v:411:y:2001:i:6839:d:10.1038_35081146
    DOI: 10.1038/35081146
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