A differential and unique expression of apoptosis-regulating Bcl-2 family proteins has been demonstrated in the rat brain during the course of development and aging. Bcl-2 is expressed highly during embryonic development but is downregulated after birth (as early as one week) (Min et al., 2003). During naturally occurring cell death (NOCD) in the rat cerebral cortex, neurons expressing Bcl-2 may determine whether a neuron dies or survives, as over-expression of Bcl-2 in transgenic mice protects neurons from NOCD (Martinou et al., 1994). Low levels of Bcl-2 protein are still present in the adult and aged brain. The sustained expression of this protein may protect neurons from various injuries or neurodegeneration. In contrast, Bcl-xL expression is maintained at a high level postnatally in the brain, suggesting that it may play an important role in the regulation of neuronal survival in the adult and aged brain (Gonzalez-Garcia et al., 1995). Bax, Bak, and Bad promote apoptosis, probably by forming heterodimers with Bcl-2 or Bcl-x, and abolishing their protective function (Davies, 1995; Yang et al., 1995). Bax and Bad expression decrease from embryonic to two to four weeks postnatal age (Vekrellis et al., 1997; Shimohama et al., 1998; Polster et al., 2003), but little is known during the development and aging of the brain. In the brain of mice, Bax is highly expressed between embryonic day 19 and one-week postnatal age of early development, but thereafter the expression dramatically declines (Min et al., 2003). In an immunochemical study, Obonai et al. showed that Bak expression in the cerebrum and cerebellum is high in the human fetuses and elderly subjects, but low in those of young adults, and suggested that Bak regulates neuronal death associated with the development and aging (Obonai et al., 1998).
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