Back Pain May Soon Be a Thing of the Past After Scientists Successfully Implant Lab-Grown Spinal Discs

This exciting new study says that you may soon be cured of that awful ache in your back.

According to the study from Penn Medicine, scientists believe we will soon be able to grow new spinal discs from a patient’s own cells as a means of replacing the deteriorated ones that cause back and neck pain.

For the first time ever, spinal discs that were grown from stem cells were successfully implanted and provided long-term function in the largest animal model ever evaluated for bioengineered disc replacement.

The soft tissues in the spinal column, the intervertebral discs, are essential for the motions of daily life, such as turning your head to tying your shoes. At any given time, however, about half the adult population in the United States is suffering from back or neck pain, for which treatment and care place a significant economic burden on society—an estimated $195 billion a year.

While spinal disc degeneration is often associated with that pain, the underlying causes of disc degeneration remain less understood. Today’s approaches, which include spinal fusion surgery and mechanical replacement devices, provide symptomatic relief, but they do not restore native disc structure, function, and range of motion, and they often have limited long-term efficacy. Thus, there is a need for new therapies.

Tissue engineering holds great promise. It involves combining the patients’ or animals’ own stems cells with biomaterial scaffolds in the lab to generate a composite structure that is then implanted into the spine to act as a replacement disc. For the last 15 years, the Penn research team has been developing a tissue engineered replacement disc, moving from in-vitro basic science endeavors to small animal models to larger animal models with an eye towards human trials – “optimistically” in the near future.

“This is a major step: to grow such a large disc in the lab, to get it into the disc space, and then to have it to start integrating with the surrounding native tissue. That’s very promising,” said Robert L. Mauck, co-senior author of the paper, which was published in Science Translational Medicine. “The current standard of care does not actually restore the disc, so our hope with this engineered device is to replace it in a biological, functional way and regain full range of motion.”

Researchers demonstrated successful total disc replacement in the goat cervical spine. They chose the goat because its cervical spinal disc dimensions are similar to humans’ and goats have the benefit of semi-upright stature. Eight weeks after the implant, MRI results suggest that disc composition was maintained or improved, and that the mechanical properties either matched or exceeded those of the native goat cervical disc.

“When you look at the success in the literature from mechanical devices, I think there is a very good reason to be optimistic that we could reach that same success, if not exceed it with the engineered discs [in humans],” said Harvey E. Smith, MD, co-senior author and clinical lead on the study.

The research team credits the success of the work to the multidisciplinary and translational approach they’ve taken since it began at Penn Medicine, which is home to the many experts from the different departments and schools who were involved in this project.

The next step will be to conduct longer-term studies to further characterize the function of the engineered discs in the goat model, the authors said, as well as model the degeneration of spinal discs in humans and to test how their engineered discs perform in that context.

“There is a lot of desirability to implant a biological device that is made of your own cells,” Smith said. “Using a true tissue-engineered motion preserving replacement device in arthroplasty of this nature is not something we have yet done in orthopaedics. I think it would be a paradigm shift for how we really treat these spinal diseases and how we approach motion sparing reconstruction of joints.”

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Can coronavirus damage the brain?

The full spectrum of the symptoms experienced by those infected with the SARS-CoV-2 is not fully known yet. Recently, research has pointed towards the neurological symptoms witnessed in COVID-19 patients.

Now, in an investigation of hospitalised COVID-19 patients in Wuhan, researchers have recorded the neurological manifestations of the disease. Their findings were published in the journal JAMA Neurology on April 10. They conclude that neurological symptoms can be noticed in a “notable proportion” of the patients and are not uncommon.

Neurological manifestations of the coronavirus (COVID-19)

In their investigation, researchers studied 214 COVID-19 patients between January 16 and February 19 and noted that over 36.4 per cent of them showed neurologic symptoms, more commonly in patients with severe infection.

They have categorised the symptoms into three categories — central nervous system manifestations which include dizziness, headache, impaired consciousness, acute cerebrovascular disease, ataxia (loss of full control of body movements) and seizures; peripheral nervous system manifestations which include taste and smell impairment, vision impairment and nerve pain; and skeletal muscular injury manifestations.
 
How can the coronavirus (COVID-19) affect the brain?

The SARS-CoV-2 virus binds itself to a receptor in the human cells called ACE2. This is also the receptor for SARS-CoV. ACE2 is present in other human organs as well, including the nervous system and skeletal muscles. Therefore, it is possible that the virus can lead to the person showing neurological symptoms through direct or indirect mechanisms using the ACE2 receptor.

Even so, it is not yet clear if the virus affects the skeletal muscles by binding with the ACE2 receptors or through some other route.

Further, the autopsy report of some COVID-19 patients showed that the brain tissue was hyperemic (congestion of blood in an organ), edematous (accumulation of watery fluids in cells or tissues) and some neurons showed degeneration.

Even so, such symptoms are not exclusive to the SARS-CoV-2 virus, neurological injury has also been reported in patients of SARS and MERS. An editorial in JAMA Neurology notes that in the case of SARS, the reports of neurological complications were limited and they appeared in patients two to three weeks into the course of illness.

So does COVID-19 affect the brain?

The researchers note that out of the 214 patients they studied, 126 had a nonsevere infection and 88 patients had severe infection. Overall, 78 patients showed neurological manifestations of the disease.

Compared to the nonsevere cases, the severe cases were older and had more comorbidities such as hypertension. Such patients also showed fewer “typical symptoms” of the disease such as fever and cough, while they were more likely to have neurological symptoms such as acute cerebrovascular disease, impaired consciousness and skeletal muscle injury.

Further, these neurological symptoms were seen early in the illness in COVID-19 patients, as opposed to similar manifestations seen in the case of some SARS patients.

Significantly, some of these patients reported themselves to the hospitals without any typical symptoms of the disease such as fever and cough, and presented themselves only with neurological symptoms. “Therefore, for patients with COVID-19, we need to pay close attention to their neurologic manifestations, especially for those with severe infections, which may have contributed to their death,” the researchers note.

An article in The New York Times said that specialists have observed neurological symptoms in COVID-19 patients in Germany, France, Austria, Italy and Holland. The report says, “Some doctors have reported cases of patients who were brought in for treatment because of their altered mental state, and who ultimately tested positive for Covid-19, although they had none of the classic symptoms like fever or cough,”, which is in line with what the researchers have observed in some patients in Wuhan as well.

Even so, further research needs to be done to understand why certain symptoms such as loss of smell or taste occur, to see if they are clinical manifestations of the disease itself or occur due to an inflammatory response in some patients.

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One type of exercise “reverses” aging’s effect on stem cells — study

As people age, they lose muscle mass and the risk of heart disease, dementia, and reduced immune function increases. As the years tick by, it becomes harder for people to bounce back from a workout, injury, or illness.

Consistent exercise can slow down this degenerative process — but a new study suggests we may not have to settle for slowing down. According to new research in mice, aerobic exercise may actually reverse aging’s effect on essential muscle stem cells involved with tissue regeneration. 

If the research translates to humans, it means jogging, swimming, cycling, and other aerobic activities can help older people recover as quickly and efficiently as their younger selves. In the far future, these results could inform the creation of a drug that de-ages muscle stem cells.

This finding was published Monday in the journal Nature Metabolism.

Researchers have known for a long time that exercise promotes healthspan, giving people extra disease-free years.

This discovery is “very different,” co-author Thomas Rando, a neurology researcher at Stanford University, tells Inverse.

“This is like taking, in a sense, a person who has already aged and acquired these diseases, and then reversed that process," Rando explains.

This study suggests that aerobic exercise can cause old cells to behave more like — and gain the characteristics of — young cells. To get there, the scientists rounded up young and old mice and gave them access to a running wheel for three weeks. Then, with a battery of tests, they analyzed how the mouse's muscle stem cells and muscle tissue responded.


They compared the mouse runners to a group of non-exercising mice who were given a locked wheel and no opportunity to run.

Within a single week, both young and old mice with the running wheels established a routine, running about 10 and 4.9 kilometers per night, respectively.

The human equivalent to the mice running wheel regime would likely be regular, aerobic exercise— swimming, running, cycling, Rando says. Not strength training or weight lifting.

After three weeks of voluntary wheel running, the mice were moved to cages without any wheels. Then, the researchers injured certain muscles and analyzed how the mice rebuilt the injured tissue.

They also transplanted muscle stem cells from old mice into other injured mice, and saw how well the cells functioned. Compared with young donor muscle stem cells, old donor muscle stem cells formed smaller and fewer fibers in the injured mice. But old muscle stem cells from exercising mice performed like young muscle stem cells, forming more fibers than non-exercising old muscle stem cells.

Overall, older mice who exercised experienced improved muscle stem cell function and accelerated muscle tissue repair.

The active, older mice didn't produce more muscle stem cells. Instead, exercise had a “rejuvenating” effect on old cells, Rando says. It triggered a Benjamin Button-effect and helped mice operate more like their younger selves.

These benefits disappeared one week after the mice stopped running, suggesting that what causes the rejuvenating effect is sustained exercise.

This implies that voluntary aerobic exercise may have benefits "above and beyond" the prevention of age-related diseases, and may actually improve tissue function directly, Rando says.

"The idea would be that that older individuals would recover faster and more efficiently like young people do in response to an injury," he explains

Surprisingly, young mice who ran the wheel did not experience improved muscle repair. This puzzled Rando and his team.

"It's as if young mice have already kind of plateaued," Rando explains. "They lose function with age and they can get back to that baseline, but it's hard to make them still better with more exercise."

Exercise’s effects on muscle stem cells and tissue repair come down to a tiny protein called cyclin D1, the study explains. Voluntary aerobic exercise restored cyclin D1 levels in dormant stem cells back to youthful levels, effectively accelerating muscle stem cell regeneration.

Discovering cyclinD1's critical role means researchers may be able to target the protein therapeutically or develop a drug that creates these positive de-aging effects, the researchers say.

But before any kind of anti-aging pill or prescribed exercise-regime comes down the pipeline, more research in humans is needed. 

Abstract: Ageing impairs tissue repair. This defect is pronounced in skeletal muscle, whose regeneration by muscle stem cells (MuSCs) is robust in young-adult animals, but inefficient in older organisms. Despite this functional decline, old MuSCs are amenable to rejuvenation through strategies that improve the systemic milieu, such as heterochronic parabiosis. One such strategy, exercise, has long been appreciated for its benefits on healthspan, but its effects on aged stem-cell function in the context of tissue regeneration are incompletely understood. Here, we show that exercise in the form of voluntary wheel running accelerates muscle repair in old mice and improves old MuSC function. Through transcriptional profiling and genetic studies, we discovered that the restoration of old MuSC activation ability hinges on restoration of Cyclin D1, whose expression declines with age in MuSCs. Pharmacologic studies revealed that Cyclin D1 maintains MuSC activation capacity by repressing TGF-β signalling. Taken together, these studies demonstrate that voluntary exercise is a practicable intervention for old MuSC rejuvenation. Furthermore, this work highlights the distinct role of Cyclin D1 in stem-cell quiescence.

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Two experimental Alzheimer's drugs show improvement in memory and anti-ageing

Researchers have found that two experimental Alzheimer's drugs, known as CMS121 and J147, improve memory and slow the degeneration of brain cells. The research suggests that the drugs may be useful for treating a broader array of conditions and points out a new pathway that links normal ageing to Alzheimer's disease. "This study further validated these two compounds not only as Alzheimer's drug candidates but also as potentially more widely useful for their anti-aging effects," said the study's co-author.

The researchers have shown how these compounds can slow ageing in healthy older mice, blocking the damage to brain cells that normally occurs during ageing and restoring the levels of specific molecules to those seen in younger brains.

Old age is the biggest risk factor for Alzheimer's disease and above the age of 65, a person's risk of developing the disease doubles about every five years.

"The contribution of old age-associated detrimental processes to the disease has been largely neglected in Alzheimer's disease drug discovery," said a staff scientist and first author of the new paper.

In the new study, the researchers turned to a strain of mice that age unusually fast.

A subset of these mice was given CMS121 or J147 beginning at nine months old -- the equivalent to late middle age in humans.

After four months, the team tested the memory and behaviour of the animals and analysed the genetic and molecular markers in their brains.

Not only did the animals given either of the drug candidates performed better on memory tests than mice that had not received any treatment, but their brains also showed differences at the cellular and molecular levels.

In particular, the expression of genes associated with the cell's energy-generating structures called mitochondria was preserved by CMS121 and J147 with ageing.

"The bottom line was that these two compounds prevent molecular changes that are associated with ageing," said the researcher.

More detailed experiments showed that both drugs affected mitochondria by increasing levels of the chemical acetyl-coenzyme A (acetyl-coA).

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Mechanism that enables brain to rapidly focus attention found

Scientists have discovered a key mechanism in the brain that may underlie our ability to rapidly focus attention.

Our brains are continuously bombarded with information from the senses, yet our level of vigilance to such input varies, allowing us to selectively focus on one conversation and not another, according to the study.

"If we want to give our full concentration, something happens in the brain to enable us to focus and filter out distractions," said a Prof.

"There must be a mechanism that signals the thing we want to focus on," said the Prof.

However, this mechanism is not well understood, he said.

Research has shown that the electrical activity of the neocortex of the brain changes when we focus our attention.

Neurons stop signalling in sync with one another and start firing out of sync.

This is helpful, he said , because it allows individual neurons to respond to sensory information in different ways.

Thus, you can focus on a car speeding down the road or on what a friend is saying in a crowded room.

It's known that the cholinergic system in the brain plays an important role in triggering this desynchronisation.

The cholinergic system consists of clusters of special neurons that synthesise and release a signalling molecule called acetylcholine, he said, and these clusters make far-reaching connections throughout the brain.

Not only does this cholinergic system act like a master switch, but mounting evidence suggests it also enables the brain to identify which sensory input is the most salient -- that is worthy of attention -- at any given moment and then shine a spotlight on that input.

"The cholinergic system broadcasts to the brain, 'this thing is really important to be vigilant to'," the Prof. said.

He added that the cholinergic system has been proposed to have a far-reaching impact on our cognitive abilities.

"Destruction of the cholinergic system in animals profoundly degrades cognition, and the formation of memory," he said.

"Importantly, in humans, progressive degeneration of the cholinergic system occurs in devastating diseases that blunt cognition and memory, such as Alzheimer's disease," he said.

However, precisely which neurons in the cortex are being targeted by this master switch and how it's able to influence their function was unknown.

Researchers wondered if layer 5 B-pyramidal neurons, the 'output' neurons of the neocortex, might be involved because they are intimately involved in how we perceive the world.

"The output neurons of the neocortex perform computations that are thought to underlie our perception of the world," said the Prof.

Researchers wanted to know if the cholinergic system is able to influence the activity of these output neurons.

Using a technique called optogenetics, they modified neurons in the cholinergic system in the brains of mice so that they could be activated with a flash of blue light, triggering a sudden release of acetylcholine.

This allowed the researchers to closely monitor the interaction between the cholinergic system and the output neurons.

They discovered that if the output neurons were not currently active, not much happened.

However, when those neurons received excitatory input to their dendrites, the cholinergic system was able to massively increase their activity.

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