Cerebrospinal fluid provides nutrients and other elements to brain cells. Scientists now show that by obtaining it from young mice and injecting it into the brains of old mice, the latter recover their memory. The effect is attributed to a protein, Fgf17, presented today in Nature as a possible brain rejuvenation factor.
Protein Fgf17 might work as a rejuvenating factor for the ageing brain.
Juan Lerma - reacción líquido cefalorraquídeo de ratones jóvenes en ratones viejos -EN
Juan Lerma
Director of the Cajal International Neuroscience Center (CINC-CSIC). Editor in chief Neuroscience.
This is a pretty good paper. It raises questions about its therapeutic scope, and about what other molecules and mechanisms may be involved in the rejuvenating effects of young cerebrospinal fluid (CSF).
The paper describes CSF as an age-determined biochemical environment that influences cognitive processes and cell survival. But they get to the heart of the matter and determine which genes, in addition to increasing oligodendrocyte proliferation and hippocampal myelination, are turned on or off when mice are treated with young CSF.
They find that it is Serum Response Factor (SRF), among others, that is stimulated. This is a transcription factor that triggers the expression of several genes related to the cytoskeleton [proteins in the cell environment] and the proliferation of oligodendrocytes [cells that form the myelin sheath that protects nerve tissues]. Genomic expression studies determine that Fgf17 (fibroblast growth factor 17) is the main factor orchestrating all this.
An interesting aspect is that, although they initially study these beneficial effects with CSF infusion from young mice, they then test CSF from young humans (24 years old) and see that it exerts the same effect in mice. In other words, the biochemical landscape that favours cognitive processes in young people and impoverishes them in older people is conserved. So this has serious translational value.
It is fortunate that Fgf17 has been identified as a key player, because it suggests that by infusing it or stimulating its synthesis we could delay the process of cognitive decline that occurs, not in pathologies such as Alzheimer's, but in the physiological one that we mature people have the opportunity to experience every day.
An ethical problem that arises is if someone with a lot of money happens to buy sources of young CSF for transfusions. Of course, this has problems, because it is not known what can be transferred with CSF besides Fgf17.
In summary, these data confirm that CSF represents a far from simple medium, whose composition has the signature of age and which determines certain cognitive qualities, through important players such as oligodendrocytes and associated factors such as SRF and Fgf17.
This opens up hope for relatively easy-to-administer treatments that can alleviate memory loss in Alzheimer's and other dementias, but also physiological connective decline. Naturally, more needs to be learned, on the one hand (basic mechanistic aspects) and on the other (to what degree this is likely to work in humans as a therapy).
