Despite accumulating evidence for the importance of apoptosis in the
pathogenesis of neurodegenerative diseases, relatively little mechanistic
information has been published to date. In an AD model, correlations
between exposure to AβP and alterations in expression of genes that are
associated with neuronal PCD in other contexts (see Section 6.4.1) have been
demonstrated. Paradis et al., for example, showed down regulation of the
antiapoptotic protein Bcl-2 and concomitant upregulation of the proapoptotic
protein Bax in AβP-treated primary human neuron cultures.210 In
another study that examined postmortem AD tissue, DNA fragmentation
(detected by TUNEL staining) was found in the same cells that displayed
increased immunoreactivity of the transcription factor c-Jun,