Can we artificially regenerate things we’ve lost, like hearing, bone, brain function, or even memories? Several new studies have revealed different repair and regeneration mechanisms in mice, sparking hope that these findings might pave the way for humans to recover things they’ve lost.
A Malaria Drug Rebuilds Bone
Bone health is a serious problem in the United States—approximately 10 million Americans have been diagnosed with osteoporosis and another 44 million have low bone density, which places them at increased risk of breaking a bone.
A new study offers hope to those with osteoporosis. Researchers at China’s Peking University International Cancer Institute found that the drug dihydroartemisinin (DHA) reduced bone loss in mouse models of osteoporosis while preserving their bone structure.
The team used an AI algorithm to search for compounds with anti-osteoporosis potential, hoping to repurpose an existing drug. The search identified DHA, a derivative of a compound called artemisinin found in the sweet wormwood plant, as a potential option. DHA is used worldwide to treat malaria.
To evaluate DHA’s effects on bone, the researchers administered extracts of the drug to mouse models of osteoporosis orally each day for six weeks. By the end of the trial period, the mice showed less bone loss and healthier bone structure than untreated mice. After a second, eight-week trial, in which the DHA was delivered in nanoparticles designed to target bone, the bones of the treated mice were almost as healthy as those of control mice.
Restoring Brain Function After Stroke
A team of researchers at Lund University in Sweden, the University of Rome La Sapienza, and Washington University at St. Louis, have discovered a way to restore brain function in rodent models of stroke.
In an ischemic stroke, blood flow to the brain is reduced, causing significant damage and nerve cell loss. This can lead to a range of symptoms, such as paralysis, pain, motor impairment, and difficulties with speech and vision.
Two days after a stroke, the team began treating mice and rats with a GluR5 inhibitor. The rodents displayed some degree of recovery within 30 minutes, but permanent recovery of sensorimotor functions required continuous treatment over several weeks.
The hope is that the mechanism could be developed into a stroke therapy for humans that could be used even days after a stroke occurs.
A different study, by researchers at Kyushu University in Japan, uncovered another method of restoring function after a stroke—turning brain immune cells into neurons.
Working with mice, the team showed that converting microglia into neurons in the brain has significant potential in treating brain injury from ischemic strokes. The treatment was effective in mice at the acute phase after stroke. Next, the team hopes to determine if the treatment works when administered in the chronic phase.
Cardiac Function Restored After Infarction
When the heart is injured, as in a heart attack, the damage is usually irreversible. Now, researchers at the Max Planck Institute for Heart and Lung Research have discovered a way to regenerate heart tissue in mice.
The team found that it could induce heart regeneration in mice by changing the energy metabolism of heart muscle cells. Using this method, heart function was largely restored.
In humans, the regenerative capacity of the heart diminishes after birth due to two factors: the inability of heart muscle cells to divide and the shift in energy metabolism from relying on sugar as an energy source to primarily using fats in a process called fatty acid oxidation.
Animals capable of heart tissue regeneration primarily use sugar as an energy source, so the researchers looked for a way to reactivate this type of energy metabolism. To accomplish this, they deactivated the Cpt1b gene, which is required for fatty acid oxidation, in mice. The hearts of the mice immediately began to regenerate, with the number of heart cells almost doubling over the course of the experiment.
Next, the team triggered a heart attack in the Cpt1b-deactivated mice. After several weeks, the heart muscles of the mice were close to their pre-heart-attack strength. Significant research is still required before a reliable treatment for humans is available, but the new finding raises the hope that heart damage may eventually be repairable in humans.
Lost Childhood Memories Recovered Using Light
Few of us have memories from before age 2, but what if there were an easy way to bring those memories back? Researchers at Trinity College Dublin have found that this specific type of memory loss may be preventable, or even reversible.
Loss of these early memories, called “infantile amnesia,” is common but not well-understood, with many people assuming it’s simply a natural function of time.
However, in a study with mice, the team investigated the molecular underpinnings of this phenomenon. They induced inflammation in pregnant mice, which is known to alter brain development and contribute to the development of autism. They found that in the mouse models of autism, infantile amnesia is not present, with the mice retaining their early memories into later life stages.
In addition, the team found that by using light to stimulate neurons in adult mice, they could restore memories from infancy, even in mice without the autism-like condition, proving that these memories are not gone but still reside in the brain.
Further research is needed to determine if the same mechanism will be effective in humans.
Regrowing Damaged Nerves
Nerve function can be lost due to injury, hereditary conditions, or aging. To date, there is no treatment for the paralysis and loss of strength that can result from nerve damage. Now, researchers at Stanford University and Sanford Burnham Prebys have successfully regenerated motor nerves after nerve injury in mice.
The team found that in mouse models of sciatic nerve damage, nerve injury results in the early expression of the enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH). By using a small molecule inhibitor to target 15-PGDH in muscle tissues, the team was able to restore nerve connectively and promote a faster recovery of muscle function and strength.
The team also detected the heightened presence of 15-PGDH in tissues of humans with a wide range of neuromuscular diseases, indicating that repressing this enzyme could be beneficial in humans with nerve damage.
A Treatment for Genetic Hearing Loss
Researchers at the University of Rochester have discovered a new way to treat genetic hearing loss.
Delivering gene therapy to the inner ear to treat hearing loss has been extremely problematic because the inner ear is difficult to access without causing damage. To address this issue, the researchers conducted a close examination of cochlear aqueducts in mice—tubes that bridge the bony walls that separate the cochlea from the brain cavity—and discovered that the channels serve to connect the fluid in the inner ear to cerebrospinal fluid.
Equipped with this new knowledge, the team was able to administer gene therapy to the mice via an injection to the base of the skull. The new technique could lead to new therapeutics for genetic hearing loss in humans.
