If you give an old mouse blood from a new one , it is almost as if the elderly rodent has been given an philosophers' stone of youth : Their organs benefit from a rejuvenating boost , and even their brains come out to take on a more vernal appearance , coinciding withimprovements in memory and eruditeness . But it also works the other way around : old bloodages the bodies of young shiner and slows their brain function .
No one is in agreement yet on why this could be , but anew studyseems to be offering some important clues . Scientists have plant a protein in our origin that increases in abundance as we get older , preventing our brain cells from regenerating and contributing to age - related cognitive descent . Importantly , if scientists can notice out a way to target this atom , then it might be possible to prevent or treat impairments in cognitive function that occur as we age .
The protein in question is called beta-2 microglobulin , or B2 M , which forms part of a larger immune molecule used to separate foreign invaders from the ego . sake was spark in B2 M after study found that mellow layer of this speck were associated with cognitive impairments in Alzheimer ’s , leading to the proposal that it could be one of the “ pro - aging factors ” in sure-enough rip that lead to the observe effects in young computer mouse .
To investigate this possibleness further , scientists from UC San Francisco and Stanford begin investigating whether its stratum changed over time . As described inNature Medicine , B2 M was found to increase with age in both mice and humans , not just in the blood but also the substance that beleaguer the brain and spinal cord , the cerebrospinal fluid ( CSF ) .
ingest this one footstep further , the squad give young shiner a social disease of B2 M , either into the blood or straight into the brain , which was discover to deflower the maturation of new brainiac cells and reduce their performance in various learning and memory test . But interestingly , after their B2 M levels reelect back to normal 30 day later , brain cell regeneration rate return to near - normal levels , and functioning on the same tests ameliorate .
Lending even further weightiness to the estimate that in high spirits B2 M level chip in to age - relate cognitive decline , old mice in which the B2 M gene had been experimentally removed were almost as skillful at learning and memory task as younger control mice . All in all , these encouraging determination raise the possibility that it might be possible to somehow block B2 thou therapeutically and cut down or reverse its contribution to the mature process .
“ From a translational perspective , we are interested in acquire antibodies or small molecules to target this protein late in life , ” lead researcher Saul Villeda said in astatement . “ Since B2 M goes up in age in blood , CSF and also in the brain itself , this allows us multiple avenue in which to aim this protein therapeutically . ”
