This study examines what in the brain influences the generation of early myelinating cells and they find that the stiffness of the tissue makes a difference. They find that a protein called PIEZO is important. This is called FAM38 in mice.
Lets hope that rodents translate to humans because the protein expression profile is different, is this because mice only last 2 years verses many more years for the humans
Niche stiffness underlies the ageing of central nervous system progenitor cells. Segel M, Neumann B, Hill MFE, Weber IP, Viscomi C, Zhao C, Young A, Agley CC, Thompson AJ, Gonzalez GA, Sharma A, Holmqvist S, Rowitch DH, Franze K, Franklin RJM, Chalut KJ. Nature. 2019 Aug 15. doi: 10.1038/s41586-019-1484-9. [Epub ahead of print]
Ageing causes a decline in tissue regeneration owing to a loss of function of adult stem cell and progenitor cell populations. One example is the deterioration of the regenerative capacity of the widespread and abundant population of central nervous system (CNS) multipotent stem cells known as oligodendrocyte progenitor cells (OPCs). A relatively overlooked potential source of this loss of function is the stem cell ‘niche’-a set of cues that include chemical and mechanical signals. The OPC microenvironment stiffens with age, and that this mechanical change is sufficient to cause age-related loss of function of OPCs. Using biological and synthetic scaffolds to mimic the stiffness of young brains, isolated aged OPCs cultured on these scaffolds are molecularly and functionally rejuvenated. When we disrupt mechanical signalling, the proliferation and differentiation rates of OPCs are increased. We identify the mechanoresponsive ion channel PIEZO1 as a key mediator of OPC mechanical signalling. Inhibiting PIEZO1 overrides mechanical signals in vivo and allows OPCs to maintain activity in the ageing CNS. We also show that PIEZO1 is important in regulating cell number during CNS development. Thus we show that tissue stiffness is a crucial regulator of ageing in OPCs, and provide insights into how the function of adult stem and progenitor cells changes with age. Our findings could be important not only for the development of regenerative therapies, but also for understanding the ageing process itself.
So the question is how do you make an old brain young, the Cambridge group may have the answer, but we will have to wait until theis reaches the shelves but they have been talking bout it for 2 years. This is more good stuff.
However, I do need to throw a scanner in the works abit. It is vital that the claiims that humans myelinate in a different t anway to rodents is addressed. The challenge has been made and at the moment the rodent myelinators are ingnoring or simply saying the former is not true. However, this challenge has come from more than one source and the data needs to be challenged properly. If not this is simply sexy science that is going nowhere