The study, published in Nature Aging, found that FTL1 builds up in the hippocampus, the brain’s memory center, as mice get older. Too much of this protein disrupts brain function. Older mice with elevated FTL1 performed poorly on memory tasks. To confirm the link, scientists boosted FTL1 in younger mice.

To confirm the link, scientists boosted FTL1 in younger mice. These healthy mice quickly developed memory problems similar to older ones. But when scientists lowered FTL1 levels in aging mice, something remarkable happened: their memory improved to the level of much younger mice.

How FTL1 Affects the Brain

FTL1 helps store iron inside cells, but when it builds up in the brain, it disrupts how neurons generate and use energy. Neurons need energy to build and maintain connections, which are the pathways for learning and memory.

When FTL1 levels rise, neurons lose power. They cannot store information as effectively, leading to forgetfulness. Scientists also observed that older mice with high FTL1 had fewer connections between brain cells.

The team used advanced tools, including viruses and genetic methods, to change FTL1 levels. They then put mice through memory and learning challenges, such as solving mazes and recognizing objects. After reducing FTL1, older mice performed almost as well as young mice, proving that brain function could be restored.

The research also tested metabolism. Researchers discovered that when FTL1 levels rise, neurons struggle to produce enough energy. When they added NADH, a compound that helps with cell energy, memory problems improved. This suggests that targeting brain energy systems could be another way to help with memory loss reversal.

What This Means for Humans

While the results are exciting, the research is still at an early stage. The experiments were done only in male mice, and the human brain is far more complex. A treatment that works in mice may not work the same way in people.

Currently, there are no safe drugs that directly reduce FTL1 in humans. The methods used in the study involved genetic tools, not medicines. Researchers warn that it could take years before this discovery leads to new therapies.

Still, the findings are important because they focus on normal, age-related memory decline, not just diseases like Alzheimer’s. Almost everyone experiences some memory loss with age. By targeting FTL1, scientists may one day find a way to help a much larger group of people.

In the United States, between six and 12 million people over 65 live with mild cognitive impairment, a condition that often leads to dementia. About one-third of them develop Alzheimer’s within five years. For these individuals, new options for memory loss reversal could make a huge difference.

A New Direction in Brain Research

For decades, dementia research has centered on proteins like beta-amyloid and tau, which form clumps and tangles in the brain. The UCSF study adds a new angle by showing that iron-related proteins and energy systems may also be key to memory decline.

By focusing on FTL1, scientists are opening doors to treatments that could help almost everyone as they grow older—not just those with Alzheimer’s disease.

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The study aimed to unravel the mystery of how women’s bones remain unaffected despite the significant loss of calcium during milk production. Traditionally, estrogen was considered crucial for bone health, but the research revealed that another factor is at play.

Senior author Dr. Holly Ingraham and her team, while studying female mice, blocked an estrogen receptor in neurons in a small brain area, resulting in increased bone mass. They suspected a blood-borne hormone but couldn’t identify it initially. An exhaustive search led to the discovery of CCN3, a hormone behaving uniquely among those secreted by neurons.

“The notion that a hormone can be secreted directly from the brain is a new concept in endocrinology,” said Ingraham. This hormone was found in lactating female mice but not the receptor, suggesting it plays a vital role in bone health during lactation.

Without CCN3, lactating female mice lost bone mass, and their offspring lost weight, highlighting the hormone’s importance. When CCN3 levels were increased in mice, both male and female, their bone mass and strength significantly improved within weeks. Remarkably, CCN3 doubled bone mass in very old female mice and those lacking estrogen.

To test its healing properties, researchers created a hydrogel patch that released CCN3 over two weeks and attached it to bone fractures in older mice. The results were astonishing: the fractures healed at the rate of young mice, a feat previously unattainable with other strategies.

Dr. Thomas Ambrosi, a project collaborator, noted, “We’ve never been able to achieve this kind of mineralization and healing outcome with any other strategy.” The hormone not only promoted healing but also supported the production of new bone cells by stem cells in the bones.

With over 200 million people affected by osteoporosis worldwide, the potential applications of CCN3 are vast. Women post-menopause, breast cancer survivors on hormone blockers, elite female athletes, and older men at higher risk of fractures could benefit from treatments based on this hormone.

“This discovery could increase bone mass in various scenarios, providing a significant breakthrough in osteoporosis and fracture treatment,” said Ingraham. Researchers plan to continue studying the molecular mechanisms of CCN3 in breastfeeding women and its broader applications in bone health.

This research opens new avenues for treating bone conditions and highlights the critical role of previously overlooked physiological mechanisms.

References:

1. Babey, M.E., Krause, W.C., Chen, K. et al. “A maternal brain hormone that builds bone.” Nature, 10 July 2024. Available from: https://doi.org/10.1038/s41586-024-07634-3.
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2. The National Institute on Aging has more about osteoporosis. University of California, San Francisco, news release, 10 July 2024. Available from: https://www.ucsf.edu/news/2024/07/429481/maternal-brain-hormone-bone-research.

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