Recent evidence indicates that alterations in brain polyamine metabolism may be critical for nerve cell survival after a free radical initiated neurodegenerative process. It has been shown previously that Aβ(1-42) and Aβ(25-35) are toxic to neurons through a free radical dependent oxidative mechanism. Treatment of rat embryonic hippocampal neuronal cultures with Aβ- peptides increased ornithine decarboxylase (ODC) activity and spermidine uptake, suggesting that oxidative stress upregulates the polyamine mechanism for the repair of free radical damage. Pretreatment of the cells with vitamin E prior to Aβ exposure decreased ODC activity and spermidine uptake to control level. This study is the first to demonstrate that Aβ treated cells show an increased polyamine metabolism in response to free radical mediated oxidative stress and that the free radical scavenger vitamin E prevents these attenuations. These results are discussed with reference to Alzheimer's disease.
|Number of pages||4|
|State||Published - Mar 1 1999|
Bibliographical noteFunding Information:
This work was supported in part by grants NIH (AG-10836; AG-05119) (D.A.B.) and NCI (CA58935) and VA Merit Review (596-0003) (K.B.A).
- Alzheimer's disease
- Amyloid β-peptide
- Free radicals
- Ornithine decarboxylase activity
- Polyamine uptake
- Vitamin E
ASJC Scopus subject areas
- Neuroscience (all)