Memory loss reversed in mice using cerebrospinal fluid from younger peers in 'pilot' study

Memory loss reversed in mice using cerebrospinal fluid from younger peers in ‘pilot’ study

Mice’s memory loss was reversed by injecting them with cerebrospinal fluid from their younger peers in a “pioneering” new treatment.

The substance, called cerebrospinal fluid (CSF), washes in and out of the gray and white matter in waves — helping to eliminate waste.

It coats tissues with proteins, or growth factors, that are vital for normal development.

Amounts decrease as we age — increasing the risk of Alzheimer’s disease and other neurological conditions.

Scientists say the treatment opens the door to new treatments and slows cognitive decline.

Using a precise tube and pump, cerebrospinal fluid (CSF) from adult mice was injected into the brains of 18-month-old animals—the equivalent of 60 in human years—over seven days.

Scans showed that it boosted the production of myelin, a fatty coating that protects nerve cells from damage.

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Next, the aged mice improved on the “fear conditioning task.” They remembered the tone and the flashing light which meant they were about to receive a small electric shock.

New hope

“Brain aging is the cause of dementia and neurodegenerative diseases, which imposes an enormous social burden,” said corresponding author Professor Tony Wyss-Coray from Stanford University in California. The improvements in memory observed in old mice receiving cerebrospinal fluid from younger animals may be attributed to growth factors that have been shown to restore neuronal function.

“Results show potential properties of young cerebrospinal fluid rejuvenation for brain aging.”

A computer tool called RNA sequencing has shown that the treatment alters gene expression in the hippocampus, which controls memory.

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It stimulates cells in the central nervous system known as oligodendrocytes. They make myelin, which ensures strong signals between nerve cells.

The study, published in Nature, found that genes normally expressed in oligodendrocytes were significantly up-regulated in aged mice treated with CSF than in young mice.

In particular, he identified the gene named Fgf17 as the main gene. Activity decreases in elderly mice.

Boosting it has achieved the same benefits as the small ± cerebrospinal fluid, giving hope for the development of a drug that targets it.

“As the brain ages, cognitive decline increases along with the risk of developing dementia and neurodegenerative diseases,” said Professor Wyss-Coray. Understanding how systemic factors affect the brain throughout life has shed light on potential treatments to slow brain aging.

“The cerebrospinal fluid is part of the immediate environment of the brain, providing nutrients to brain cells, signaling molecules and growth factors.”

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Age-related cognitive decline affects up to a quarter of people over the age of 60. A healthy diet and regular exercise protect against this – but there are no drug treatments.

Pioneering treatment

Professor Wyss-Coray said these findings demonstrate the regenerative power of young cerebrospinal fluid and identify Fgf17 as a key target for restoring the function of oligodendrocytes in the aging brain. Taken together, our results suggest that targeting myelogenesis in the hippocampus by factors in the small cerebrospinal fluid may be a therapeutic strategy to prevent or rescue cognitive decline associated with aging and neurodegenerative diseases.

Dr. Miriam Zawadzky and Professor Maria Lehtinen, of Boston Children’s Hospital in Massachusetts, who were not involved in the study, called the study “pioneering.”

“Not only does the study indicate that FGF17 has potential as a treatment
goal, but also suggests ways to administer drugs that allow for treatments
Direct access to cerebrospinal fluid may be useful in treating dementia.” “Any such treatment would be very useful in supporting our aging population.”

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2022-05-12 16:01:29

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