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pubmed:abstractText |
We have previously examined the involvement of the B cell leukemia-2 gene product (Bcl-2) family proteins (Bcl-2, Bcl-x, Bax, Bak, and Bad) in Alzheimer's disease (AD) and found that Bcl-2, Bcl-x, Bak, and Bad were upregulated. As AD is an aging-associated disease, in the present study we examined the developmental and aging-related changes in Bcl-2 family proteins in the rat brain. Immunoblot analyses of brain extracts from embryonic day 19 (E19) to postnatal 96-week-old rats indicated that the Bcl-2 protein level was highest at E19 and decreased after birth. Bcl-x levels remained high from E19 to 96 weeks. Bax levels were high from E19 to 2 weeks and decreased from 4 weeks onward. Bak levels were highest at E19 and decreased abruptly after birth. Bad levels were high from E19 to 2 weeks and decreased abruptly at 4 weeks. The present results suggest that the expression of each Bcl-2 family protein is differentially regulated during development and aging and that the changes in the senescent brains are different from those observed in AD.
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