Blocking "Pro-Aging" Molecule Could Reverse Memory Loss

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If you give an old mouse blood from a young one, it is almost as if the elderly rodent has been given an elixir of youth: Their organs benefit from a rejuvenating boost, and even their brains start to take on a more youthful appearance, coinciding with improvements in memory and learning. But it also works the other way around: old blood ages the bodies of young mice and slows their brain function.

No one is in agreement yet on why this could be, but a new study seems to be offering some important clues. Scientists have found a protein in our blood that increases in abundance as we get older, preventing our brain cells from regenerating and contributing to age-related cognitive decline. Importantly, if scientists can find out a way to target this molecule, 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 B2M, which forms part of a larger immune molecule used to distinguish foreign invaders from the self. Interest was sparked in B2M after studies found that high levels of this molecule were associated with cognitive impairments in Alzheimer’s, leading to the proposal that it could be one of the “pro-aging factors” in old blood that contributes to the observed effects in young mice.

To investigate this possibility further, scientists from UC San Francisco and Stanford began investigating whether its levels changed over time. As described in Nature Medicine, B2M was found to increase with age in both mice and humans, not just in the blood but also the substance that surrounds the brain and spinal cord, the cerebrospinal fluid (CSF).

Taking this one step further, the team gave young mice a dose of B2M, either into the blood or directly into the brain, which was found to impair the growth of new brain cells and reduce their performance in various learning and memory tests. But interestingly, after their B2M levels returned back to normal 30 days later, brain cell regeneration rates returned to near-normal levels, and performance on the same tests improved.

Lending even further weight to the idea that high B2M levels contribute to age-related cognitive decline, old mice in which the B2M gene had been experimentally removed were almost as adept at learning and memory tasks as younger control mice. All in all, these encouraging findings raise the possibility that it might be possible to somehow block B2M therapeutically and reduce or reverse its contribution to the aging process.

“From a translational perspective, we are interested in developing antibodies or small molecules to target this protein late in life,” lead researcher Saul Villeda said in a statement. “Since B2M goes up in age in blood, CSF and also in the brain itself, this allows us multiple avenues in which to target this protein therapeutically.”

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