Abstract
DNA damage has been documented in neurodegenerative conditions ranging from Alzheimer's disease to stroke. DNA-dependent protein kinase (DNA-PK) is involved in V(D)J recombination and DNA double strand break repair, and may play a role in cell death induced by DNA damage. We now report that cultured hippocampal neurons from severe combined immunodeficient (scid) mice which lack DNA-PK activity are hypersensitive to apoptosis induced by exposure to topoisomerase inhibitors, amyloid beta peptide (Aβ) and glutamate. A similar increased vulnerability of hippocampal CA1 and CA3 neurons was observed in adult scid mice after kainate-induced seizures. Our results suggest that DNA-PK activity is important for neuron survival under conditions that may occur in neurological disorders.
| Original language | English |
|---|---|
| Pages (from-to) | 257-262 |
| Number of pages | 6 |
| Journal | Molecular Brain Research |
| Volume | 87 |
| Issue number | 2 |
| DOIs | |
| State | Published - Mar 5 2001 |
Bibliographical note
Funding Information:The authors thank S.W. Crump, M. Killen and J. Partin for excellent technical support. The present study was supported by the NIA and by a DFG grant to C.C. (CU 43/1-1).
Keywords
- Alzheimer's disease
- Amyloid beta-peptide
- DNA repair
- Epileptic seizure
- Glutamate
- Topoisomerase inhibitor
ASJC Scopus subject areas
- Molecular Biology
- Cellular and Molecular Neuroscience