1) Organisms age for the good of the survival of the species. This is largely based on observations of animals like salmon, who swim uphill to fertilize eggs and then die. This theory doesn’t hold up formally, falling victim to the tragedy of group selectionism.
2) Rate-of-living. This is the idea that you have a certain amount of metabolic potential, and you can either use it up quickly or use it slow and live a long time. Metabolizing creates collatereal damage that harms cells and leads to aging. Some evidence is lizards and turkeys, which have slow metabolic rates and comparatively live a long time. Also, the accumulation of metabolic toxins like free radicals is bad for your tissues. Therefore, downregulating genes that produce free-radicals should improve lifespan, and that is the case in Drospholia. Caloric restriction can also increase lifespan in C. elegans and some other species. However, cellular metabolic rate is comprapable in species while lifespan is not, so it does not actually inversely correlate with lifespan. Bats for instance have a high cellular metabolic rate and live a very long time. This theory may have some truth on some macro level but the proposed mechanism is somewhat shaky.
3) Evolutionary theory of aging. Genes whose function is essential for reaching and aiding during reproductive maturity might benefit the fitness of the organism but harm the animal in later life stages. These genes might be selected for despite their deleterious effects because by that point the animal would already have reproduced. For example, testosterone is good for reproductive success in males, but it inhibits immune function, arterial repair, and molecular DNA repair. A positive expression for the polymorphic ApoE allele E4 leads to higher incidence rates of Alzheimer’s, which doesn’t make sense evolutionarily without this theory. Within this context, it is likely that the positive expression of the allele either has a positive effect on reproductive success early in the lifespan or at least is under very little selection pressure to be eliminated.
What does this have to do with the brain? Hormone regulation is done via the thalamus and pituitary gland, and hunger regulation is in the hypothalamus. Hormones like leptin control caloric intake and insulin release: the former is implicated via the evidence for the rate-of-living theory and the latter of which has been implicated as determining lifespan in some animal models. Also, the brain controls circaadian rhythms, which could be involved in lifespan for obvious reasons.
In C. elegans, Wolkow et al (2000) found that daf-2 mutants have much longer lifespans than wildtype specimens (10.3 +/- 1.9 days for WT and 28.8 +/ 4.8 for mutants). This lifespan increase is brought back down to more normal levels if daf-2 is expressed via a unc-14 reinsertion in neurons (16.8 +/ 3.9), but not if it is reinserted via the unc-54 in muscle cells (24.9 +/- 9.3). This suggests that the nervous system plays a large role in regulating lifespan even in simple nervous systems such as C. elegans, and signifies that the brain is an obvious place to conduct further aging research.
Wolkow CA, Kimura DK, Lee M-S, Ruvkun G. 2000 Regulation of C. elegans life-span by insulin-like signaling in the nervous system. Science 290:147-150.
Braeckman BP, Houthoofd K, Vanfleteren JR. 2000 Insulin-like signaling, metabolism, stress resistance and aging in Caenorhabditis elegans. Mechanisms of Aging and Development 122:673-693.