Part 2 of my answer that began in the previous post:
It is actually not known if a maximum lifespan exists for any postmitotic cells of mammals, including neurons.
To address this issue, scientists published in the top journal PNAS a study that exploited the differences in maximum lifespan of different strains of mice and rats.
In short neurons from mice lived twice as long as the mice live - when transplanted into longer lived rats.
While we are not rodents, this *supports the conjecture that your mammalian brain could live significantly longer if your old body is switched out to a young one.
“The lifespan of neurons is not limited by the maximum lifespan of the donor organism, but continues when transplanted in a longer-living host,” according to the study, published in the Proceedings of the National Academy of Sciences
From the actual paper:
Lifespan of neurons is uncoupled from organismal lifespan
Neurons in mammals do not undergo replicative aging, and, in absence of pathologic conditions, their lifespan is limited only by the maximum lifespan of the organism.
Whether neuronal lifespan is determined by the strain-specific lifetime or can be extended beyond this limit is unknown. Here, we transplanted embryonic mouse cerebellar precursors into the developing brain of the longer-living Wistar rats. The donor cells integrated into the rat cerebellum developing into mature neurons while retaining mouse-specific morphometric traits. In their new environment, the grafted mouse neurons did not die at or before the maximum lifespan of their strain of origin* but survived as long as 36 mo, doubling the average lifespan of the donor mice.
Thus, the lifespan of neurons is not limited by the maximum lifespan of the donor organism, but continues when transplanted in a longer-living host.
Our results suggest that mouse cerebellar neural and glial precursors, xenotransplanted into the rat CNS, integrate into the host tissue and differentiate, maintaining species-specific morphometric traits, but survive as long as the surrounding host rat neurons, doubling their expected average survival in the mouse.
Those increases are larger than the relative increases in organismal lifespan induced in mice by dietary (30), pharmacologic (31), and most genetic manipulations (32)
Our results suggest that neuronal survival and aging are coincidental but separable processes, thus increasing our hope that extending organismal lifespan by dietary, behavioral, and pharmacologic interventions will not necessarily result in a neuronally depleted brain.
