Abstract
INTRODUCTION. On the one hand, the molecular basis of the selective neuronal vulnerability in Alzheimer's disease (AD) is still largely unknown despite intense research over the last decades. On the other hand, it was recently found that the aging mouse brain shows among others parallels with human neurodegenerative disorders at the transcriptional level (1). Since both a decline of nuclear (n) DNA repair capacity and mitochondrial (mt) dysfunction have been demonstrated to be important aspects of the pathogenesis of AD, we have studied the extent of nDNA repair and mtDNA synthesis in the aging mouse brain quantitatively, specific for different cell types and in situ.
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