The tumor suppressor protein p53 has been described "as the guardian of the 
genome" for its crucial role in regulating the transcription of numerous genes 
responsible for cells cycle arrest, senescence, or apoptosis in response to 
various stress signals. Although p53 promotes longevity by decreasing the risk 
of cancer through activation of apoptosis or cellular senescence, several 
findings suggest that an increase of its activity may have deleterious effects 
leading to selected aspects of the aging phenotype and neurodegenerative 
diseases. There is the link between p53 and oxidative stress, the latter a 
crucial factor that contributes to neurodegenerative processes like Alzheimer 
disease (AD). In the present study, using a proteomics approach, we analyzed the 
impact of lack of p53 on the expression of several brain mitochondrial proteins 
involved in different pathways, and how lack of p53 may present a target to 
restore neuronal impairments. Our investigation on isolated brain mitochondria 
from p53((-/-)) mice also provides a better understanding of the 
p53-mitochondria relationship and its involvement in the development of many 
diseases.