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Impaired p53 pathway in Alzheimer's

Free radicals are often generated during normal metabolism and can cause oxidative stress and DNA damage. Cells respond by halting the cell cycle to allow DNA to be repaired or to undergo apoptosis. These free radicals appear to be risk factors in Alzheimer's disease (AD) and might contribute to initiation and progression of neurodegeneration. To investigate this link, Maurizio Memo and co-workers have compared the effects of exposure to hydrogen peroxide on fibroblasts from sporadic AD patients and fibroblasts from individuals who do not have the disease (see p. 3131). They find that the AD fibroblasts exhibit reduced cell cycle arrest and re-enter the cell cycle more quickly in response to hydrogen peroxide — despite levels of DNA damage similar to those of non-AD fibroblasts. In addition, the AD fibroblasts are less likely to undergo apoptosis. The authors show that this is because peroxide-induced activation of the tumour suppressor p53 and its apoptotic target genes (e.g. Bax) is impaired in AD fibroblasts. Such an inability to respond correctly to free-radical-induced DNA damage could play an important role in neurodegeneration.

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Selective impairment of p53-mediated cell death in fibroblasts from sporadic Alzheimer's disease patients

Daniela Uberti, Teresina Carsana, Enza Bernardi, Luigi Rodella, Piergiovanni Grigolato, Cristina Lanni, Marco Racchi, Stefano Govoni, and Maurizio Memo
JCS 2002 115: 3131-3138. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?