Groundbreaking studies by scientists at the University of California in the United States have found that blocking certain receptors in the brain leads to the growth of remarkably strong bones in mice. The results from the studies if replicated and trialed successfully in people could potentially have far-reaching significance in the treatment of osteoporosis and other bone-wasting diseases.

Osteoporosis occurs from the gradual decrease of bone density. In a healthy person, the body breaks down old or damaged bone and replaces it with new bone. However, as we age, this cycle slows down, and the body breaks down more bone than can be remade. At present there is no cure for osteoporosis or for slowing the progress of the disease, with treatments focusing on reducing the risk of fractures.

Osteoporosis affects both men and women, but is most likely to occur in women after menopause, because of the sudden decrease in estrogen, the hormone that normally protects against osteoporosis. Estrogen has a wide range of functions in the human body, particularly in regard to reproduction, and in the brain where its functions are less well known. Recently, researchers at California University studying estrogen in the brain and the role it plays in altering metabolism during different stages of life, made a serendipitous discovery that links the hormone to osteoporosis.

The scientists were focusing on estrogen-sensitive neurons in the hypothalamus — the region of the brain that links the nervous system to the endocrine (hormone) system. The hypothalamus plays an important part in regulating metabolic processes, such as controlling body temperature, hunger, sleep, fatigue and circadian rhythms.

When the scientists blocked the effects of estrogen in the hypothalamus of mice, the animals gained weight and became less active. They also discovered that the extra weight was due to increased bone mass, with some of the mice increasing their total bone mass by 800 percent. While in the blood, estrogen promotes bone growth; in the hypothalamus, they clearly appeared to have the opposite effect.

Scientists were thrilled, especially since bone mass gain was discovered only in female mice, potentially pointing to a new pathway that could be used to improve bone strength in older women and in others with fragile bones. The researchers then extended their experiments to understand how bone density changed during the lifespan of a mouse. They noticed that bone density was maintained throughout old age in mice whose estrogen receptor cells were blocked.

Additionally, when scientists deleted estrogen receptors in mice suffering from a mouse model of osteoporosis, where the mice had lost 70 percent of their bone mass, they found that bone density rebounded by 50 percent in just a few weeks.

Scientists now believe that after puberty, the estrogen system in the female brain actively shifts resources away from bone growth and towards things like reproduction, which could contribute to higher risk of weakened bones in females as they age.

Since the results are surprising and novel, more work will be needed; however, they have already opened some exciting new avenues for osteoporosis, including the chance of developing a drug that counteracts osteoporosis, said the researchers.

 


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