Changing cerebrospinal fluid can improve memory? Scientists find that memory is not only related to the depth of brain convolution

Original title: Changing your cerebrospinal fluid will improve your memory?

Scientists have found that memory improvements in old mice infused with cerebrospinal fluid (CSF) from young mice may be due to growth factors that have the ability to restore nerve cell function. The relevant research results were published in Nature on May 11, which demonstrated the potential regenerative properties of young mouse CSF for the aging brain.

As the brain ages, cognitive decline worsens with an increased risk of dementia and neurodegenerative diseases. Understanding the impact of systemic factors on the brain throughout life can provide new insights into the development of potential therapies to slow brain aging. Cerebrospinal fluid is part of the brain's immediate environment, responsible for delivering nutrients to brain cells and transducing signals of various molecules and growth factors, but the role of cerebrospinal fluid in brain aging has not been fully understood.

To test the potential regenerative properties of cerebrospinal fluid, Tony Wyss-Coray and colleagues at Stanford University in California, USA, perfused cerebrospinal fluid from young mice (10 weeks old) into the brains of old mice (18 months old). The authors reported that this treatment improved memory function in the old mice. The study showed that cerebrospinal fluid from young mice can enhance the stimulation of oligodendrocyte precursor cells in the hippocampus (the memory center of the brain), and has the potential to regenerate oligodendrocytes (a type of nerve cell) and myelin (a fatty substance that protects nerve cells).

To clarify the mechanism behind these effects, the authors investigated the signaling pathways activated by the cerebrospinal fluid of young mice. The study showed that a transcription factor called SRF mediates the effects of the cerebrospinal fluid of young mice on oligodendrocyte precursor cells and that its expression decreases in the hippocampus of old mice.

The authors also found that a growth factor called Fgf17 is a candidate molecule for inducing SRF signaling. The expression level of Fgf17 was shown to decrease in aged mice. However, injection of Fgf17 into old mice recapitulated the effects of perfusing cerebrospinal fluid from young mice, including the induction of oligodendrocyte precursor cell proliferation and improved memory function.

The authors concluded that the findings suggest that Fgf17 is a potential factor promoting regeneration in the aged brain.

"This study not only suggests the potential of the FGF17 gene as a therapeutic target, but also shows the possible benefits of a drug delivery route that allows direct access to the cerebrospinal fluid for the treatment of dementia," Miriam Zawadzki and Maria Lehtinen of Boston Children's Hospital in Massachusetts wrote in a news and opinion article published simultaneously.