Posts Tagged ‘medicine’


At this moment, there are 115,000 Americans who will die if they don’t get matched with a donated organ. Twenty of them die every day, according to data collected by the United Network for Organ Sharing (UNOS).

Part of the reason that waiting list is so long is because (surprise) organs don’t fare too well without a warm, gooey body keeping them safe. Both a liver and pancreas, for which the UNOS says 14,000 and 900 people respectively are currently waiting, can only be transplanted within twelve hours of donation. Another 4,000 people are waiting for a new heart, but those only last six hours outside the body before they begin to decay.

The 95,000 people waiting on a kidney donation get a little bit more wiggle room — those can last about 30 hours. But considering all of the logistical hurdles and difficulties of matching, donating, transporting, and, transplanting organs, recipients need to be ready for surgery more or less immediately once one is available.

The simplest way to get more organs to the people who need them, it would seem, is to freeze donated organs until they’re needed, like you might do with a casserole.

It’s such a simple idea that scientists and doctors came up with the idea decades ago, but they encountered two major roadblocks that seemed insurmountable — at least, until very recently.

The doctors, cryobiologists, engineers, and physicists at biotech company Arigos Biomedical may have come up with a way to freeze and store organs for as long as necessary. The company, previously funded by two of Peter Thiel’s science-focused foundations, recently raised just under $1 million in a seed round (participants included a venture firm, an angel investor and a family foundation, they note). Arigos co-founder and CEO Tanya Jones tells Futurism that they hope to begin human experiments as soon as 2020; if that goes well the technique could be used in clinics five to seven years after that.

If their technology works, it could shorten or even eliminate some of the organ transplant waitlists in America and around the world.

To understand the science that makes this possible, we need to look at why cryopreservation hasn’t worked in the past.

The first hurdle that cryobiologists need to overcome happens while the organ is on its way down to -120 degrees Celsius, the temperature at which molecular activity stops and organs can be stored indefinitely. People, you may recall, are mostly water, and when water freezes it expands into solid ice. This fact can cause problems as organs freeze, since congealing ice pulls water from nearby cells that need it and can rupture blood vessels as it expands. This is especially a problem since expansion and freezing happen at different times as organs freeze from the outside in.

The second hurdle comes during the warming process: just like an ice cube thrown into a glass of lukewarm water, organs tended to fracture and pop as they thawed. Not too helpful if you’re trying to replace a leaky lung or heart with a non-leaky one.

Scientists solved the first problem, Jones told Futurism, in the 1970s when they discovered a process called vitrification: pumping a cocktail of organic compounds into the organs pulled out most of the water. The remaining solution — water mixed with the added organic molecules — was so full of ­­stuff that it didn’t form ice. Instead, it froze into a type of solid glass that didn’t damage the organs the way ice did. As a result, organs could be frozen without worrying about harmful ice buildup.

But many solutions used in vitrification ended up being toxic. And the second problem, the fracturing issue, still eluded scientists. Over the following decades, most lost hope and gave up.

Jones says that she and Arigos cofounder Stephen Van Sickle found a new solution when Van Sickle took a trip to the library and realized how many old research papers chronicled the attempts to prevent fracturing.

“He went to a library and uncovered a line of old research in the transplant world that was abandoned,” says Jones.

They found a way to flush out all the arteries and veins of the organ and replace it with gas. In the past, scientists had tried replacing the blood and liquid found in a donated heart with oxygen gas, which gave the organs a little bit of extra support and padding as they grew rigid. The field then shifted towards liquids. These liquid perfusions tended to work a little bit better but left the realm of gas cushions as an unexplored loose end.

Jones and Van Sickle decided gas was worth a shot — helium gas in particular, because it wouldn’t be toxic to the donated organs. “You could use any inert noble gas because rule number one: absolutely no dying [it doesn’t kill organs], and rule number two: no blowing up the lab,” says Jones. In helium, they found a way to uniformly cool an organ and also provide its vasculature with some cushioning so that any stress built up during the cooling process wouldn’t cause a fracture. With helium gas in its veins and arteries, an organ is free to shift as it freezes without shattering, just as skyscrapers are engineered to sway rather than topple in the wind.

When they realized that no one else had tried helium, Arigos was born. And it worked really well. Soon their methods became the only way to successfully freeze and thaw organs from any animal larger than a rabbit.

“We have recovered pig kidneys from temperatures of -120 degrees Celsius, which is basically the glass transition temperature,” Jones says. “We tested on pig hearts, and it worked so well and so quickly that we were unexpectedly unprepared to test the recovery.” To be more prepared in the future, the team is working on automating its processes.

Ideally, the technique could create a universal bank of donated organs so that people could be matched with an organ right when they need it, rather than having to wait their turn in line until a suitable match turns up. Or, at least, it could make it much easier to get organs to the people who need them.

A bank of frozen organs could help solve some of the more banal (but very real) hurdles to transplantation. For example, donors and recipients sometimes have different immune systems. It’s more than just their blood types — before a transplant, doctors need to see how many of the six relevant antigens (molecules that can trigger the immune system into rejecting an organ) match up as well.

With a bank of frozen organs at the ready, doctors would be able to not only save more lives with organ transplants, but they could also more carefully match donated organs and recipients to prevent rejection because a better match could be readily available in the freezer.

But it needs FDA approval to make that happen. The company plans to conduct its first pig transplant in 2019, which it hopes will go well enough to convince the FDA to authorize a human trial in 2020. From there, it will take five to seven years for federal approval.

Others in the organ transplantation community are skeptical that Arigos can achieve everything that it claims to do, especially in the timeframe it set out.

“I would predict it would be longer than that, to actual human trials,” David Klassen, Chief Medical Officer at UNOS, tells Futurism. Normally there needs to be a great deal of animal experimentation before human testing is authorized, Klassen says, and these things take time. “That’s guessing on my part, but I would expect it would be a little longer than two years before human trials.”

But still, Klassen says that that the results coming out of organ freezing research are promising, and that he hopes to see continued interest in freezing organs.

“In broad strokes, I do think it is a top priority and should be. I think from the perspective of clinical transplantation, that whole area is a little underappreciated by people who work in the field day to day,” he says. But in the distant future, he also hopes to see the research community move beyond organ banking and develop ways to 3D print or construct organs from scratch, ultimately eliminating the need for donors in the first place.

But not everyone is convinced that cryopreservation is the future of organ transplantation at all, or that Arigos is the company to do it. Robert Kormos, director of the artificial heart program and co-director of the heart transplantation program at the University of Pittsburgh Medical Center, told Futurism that he’s skeptical of organ freezing technology.

“I went to [Arigos Biomedical’s] website and there’s a lot of claims of what they’re purporting to do and what they want to do, but usually what companies like this do is give you a list of publications so you can look at what’s been published in this area,” Kormos says. The lack of published research, completed by either by Arigos staff or other researchers in the field at large, raised a red flag for Kormos, who adds that he has not seen a lot of progress in organ freezing research, a field that he’s seen slow down over the decades.

“This company may have something, but again I’m eager to see what science they’re bringing to the table,” he says. “I think cryopreservation is an interesting concept, but we’re a ways away from that being reality. Again, I haven’t seen the data.”

Until their technique is approved, Arigos is working with some collaborators to improve the way scientists develop new pharmaceuticals. Right now, it’s difficult to bring new drugs to the market because many compounds that work great in animal studies don’t work the same way in humans. As a result, one in five phase I clinical trials, the first of three types of experiments conducted on humans before a drug can be approved, typically fails.

Arigos is planning to sell some slices of frozen, donated human organs to pharmaceutical researchers. That could help researchers determine whether or not a drug is toxic to people before they try it in a full-fledged experiment.

“We’ve got some collaborators set up who are going to explore that with us once we get access to human hearts, which we don’t quite yet,” says Jones.

But even if Arigos’ human trials are successful, the company won’t be able to store every type of organ that someone might need. Because their technique requires filling blood vessels with helium, it doesn’t work so well on organs that don’t have blood vessels, so they’ve only been able to freeze and store organs such as kidneys, livers, hearts, and lungs.

The military would love to be able to store entire frozen limbs, but that’s not on the table right now. If a soldier were to lose a limb after being caught in an explosion, it would be helpful to be able to freeze that limb until it’s ready to be reattached. That would give the soldier time to recover before undergoing surgery.

Freezing technology can’t help there yet. Bone tissue doesn’t take up the cryoprotectant solution well. And there are so many different tissue and cell types in a whole limb, each of which has a different tolerance level to the somewhat-toxic vitrification solution, that the technique wouldn’t really work. Arigos’ technique also wouldn’t work on transplantable corneas since they also have no vasculature, so scientists will need to develop new techniques if we want a universal bank of donated organs.

This also means, as Jones explained, that Arigos’ technology will not allow (presumably very rich) people to totally freeze their bodies and re-emerge in the distant future, as so many sci-fi stories have assured us will be possible. No, Arigos’ focus is strictly on medical uses for frozen organs.

If things go the way Arigos hopes, people worldwide could benefit. “There some countries in the world that don’t even have transplant technology,” says Jones. Aside from the immediate benefits to Americans stuck on an endless waitlist for the next kidney, frozen organs could be shipped or stored anywhere, bringing aid to countries and regions where there’s no waitlist at all.



A machine learning-based model using data routinely gathered in primary care identified patients with dementia in such settings, according to research recently published in BJGP Open.

“Improving dementia care through increased and timely diagnosis is a priority, yet almost half of those living with dementia do not receive a timely diagnosis,” Emmanuel A. Jammeh, PhD, of the science and engineering department at Plymouth University in the United Kingdom, and colleagues wrote.

“A cost-effective tool that can be used by [primary care providers] to identify patients likely to be living with dementia, based only on routine data would be extremely useful. Such a tool could be used to select high-risk patients who could be invited for targeted screening,” they added.

The researchers used Read codes, a set of clinical terms used in the U.K. to summarize data for general practice, to develop a machine learning-based model to identify patients with dementia. The Read codes were selected based on their significant association with patients with dementia, and included codes for risk factors, symptoms and behaviors that are collected in primary care. To test the model, researchers collected Read-encoded data from 26,483 patients living in England aged 65 years and older.

Jammeh and colleagues found that their machine-based model achieved a sensitivity of 84.47% and a specificity of 86.67% for identifying dementia.

“This is the first demonstration of a machine-learning approach to identifying dementia using routinely collected [National Health Service] data, researchers wrote.

“With the expected growth in dementia prevalence, the number of specialist memory clinics may be insufficient to meet the expected demand for diagnosis. Furthermore, although current ‘gold standards’ in dementia diagnosis may be effective, they involve the use of expensive neuroimaging (for example, positron emission tomography scans) and time-consuming neuropsychological assessments which is not ideal for routine screening of dementia,” they continued.

The model will be evaluated with other datasets, and have its validation tested “more extensively” at general practitioner practices in the future, Jammeh and colleagues added. – by Janel Miller

Diagram of the brain of a person with Alzheimer’s Disease.

In recent years, researchers have largely converged on the role of inflammation in the development and progression of Alzheimer’s disease (AD). Studies over the past decade have revealed unexpected interactions between the brain and the immune system, and metabolic conditions such as obesity and diabetes may activate inflammatory responses that contribute to the development and progression of AD.

The activation of the inflammatory response is controlled by the inflammasome, a multi-protein oligomer that promotes the release of several pro-inflammatory cytokines including interleukin 1β (IL-1β) and interleukin 18 (IL-18). In an earlier study, a group of researchers with the University of Massachusetts Medical School, the University of Tokyo and the University of Bonn reported that mice with a cognate of Alzheimer’s disease that were additionally bred to knock out the NLRP3 gene encoding the inflammasome were completely protected from neurodegenerative effects of the disease. The researchers presumed that this was the result of their inability to produce IL-1β and IL-18.

This finding was quite promising, suggesting that targeting components of the inflammasome might be a path to Alzheimer’s treatments. In their new study, they sought to determine the effect of IL-18 by breeding IL-18 knockout mice. The researchers considered IL-18 to be a promising target, because levels are elevated in the cerebrospinal fluid of AD patients with mild cognitive impairment. Additionally, it is known to increase the production of amyloid peptide.

But the result of the new mouse study was startling, and completely unprecedented in Alzheimer’s research. The IL-18 knockout mice developed a lethal seizure disorder that the researchers attribute to an increase in neuronal network transmission. The authors write, “… the effects of IL-18 deletion were so dramatic that we were unable to identify previous evidence to help understand the phenomena.”

The finding that a proinflammatory cytokine might in some way ameliorate seizure-inducing neural activity seems counterintuitive, since inflammation is theorized to promote neurodegenerative symptoms in AD. The researchers believe that epilepsy is understudied in AD patients, even though it is a common complication; they point out that two-thirds of AD patients experience both motor and non-motor seizures. Additionally, AD patients with epilepsy are more likely to develop memory loss and other cognitive symptoms, and experience a more widespread loss of brain cells than AD patients without epilepsy, according to the researchers.

They theorize that IL-18 may be counteracting seizure-promoting effects of IL-1β, and suppressing IL-18 thus induced seizures in the test mice. “In fact,” they write, “the countereffect of IL-18 and IL-1β has been documented in a mouse model of cerebellar ataxia. Importantly, we found that the acute application of IL-18 protein reduced excitatory synaptic transmission in the hippocampus, providing evidence that IL-18 has a protective function in neuronal excitability. Thus, we speculate that IL-18 directly suppresses these proepileptogenic effects of IL-1β in APP/PS1 mice.”

However, the most important implication of the study may be that, while the inflammasome is a promising therapeutic target for Alzheimer’s, inhibiting specific cytokines could negatively affect people with the disease.

More information: Inflammasome-derived cytokine IL18 suppresses amyloid-induced seizures in Alzheimer-prone mice. Proceedings of the National Academy of Sciences (2018).

Alzheimer’s disease (AD) is characterized by the progressive destruction and dysfunction of central neurons. AD patients commonly have unprovoked seizures compared with age-matched controls. Amyloid peptide-related inflammation is thought to be an important aspect of AD pathogenesis. We previously reported that NLRP3 inflammasome KO mice, when bred into APPswe/PS1ΔE9 (APP/PS1) mice, are completely protected from amyloid-induced AD-like disease, presumably because they cannot produce mature IL1β or IL18. To test the role of IL18, we bred IL18KO mice with APP/PS1 mice. Surprisingly, IL18KO/APP/PS1 mice developed a lethal seizure disorder that was completely reversed by the anticonvulsant levetiracetam. IL18-deficient AD mice showed a lower threshold in chemically induced seizures and a selective increase in gene expression related to increased neuronal activity. IL18-deficient AD mice exhibited increased excitatory synaptic proteins, spine density, and basal excitatory synaptic transmission that contributed to seizure activity. This study identifies a role for IL18 in suppressing aberrant neuronal transmission in AD.
Journal reference: Proceedings of the National Academy of Sciences


Researchers have identified a brand new ‘micro-organ’ inside the immune system of mice and humans – the first discovery of its kind for decades – and it could put scientists on the path to developing more effective vaccines in the future.

Vaccines are based on centuries of research showing that once the body has encountered a specific type of infection, it’s better able to defend against it next time. And this new research suggests this new micro-organ could be key to how our body ‘remembers’ immunity.

The researchers from the Garvan Institute of Medical Research in Australia spotted thin, flat structures on top of the immune system’s lymph nodes in mice, which they’ve dubbed “subcapsular proliferative foci” (or SPFs for short).

These SPFs appear to work like biological headquarters for planning a counter-attack to infection.

Immune cells gathering at the SPF, with the purple band showing the SPF surface.

These SPFs only appear when the mice immune systems are fighting off infections that have been encountered before.

What’s more, the researchers detected SPFs in human lymph nodes too, suggesting our bodies react in the same way.

“When you’re fighting bacteria that can double in number every 20 to 30 minutes, every moment matters,” says senior researcher Tri Phan. “To put it bluntly, if your immune system takes too long to assemble the tools to fight the infection, you die.”

“This is why vaccines are so important. Vaccination trains the immune system, so that it can make antibodies very rapidly when an infection reappears. Until now we didn’t know how and where this happened.”

Traditional microscopy approaches analyse thin 2D slices of tissue, and the researchers think that’s why SPFs haven’t been spotted before – they themselves are very thin, and they only appear temporarily.

In this case the team made the equivalent of a 3D movie of the immune system in action, which revealed the collection of many different types of immune cell in these SPFs. The researchers describe them as a “one-stop shop” for fighting off remembered infections, and fighting them quickly.

Crucially, the collection of immune cells spotted by the researchers included Memory B type cells – cells which tell the immune system how to fight off a particular infection. Memory B cells then turn into plasma cells to produce antibodies and do the actual work of tackling the threat.

“It was exciting to see the memory B cells being activated and clustering in this new structure that had never been seen before,” says one of the team, Imogen Moran.

“We could see them moving around, interacting with all these other immune cells and turning into plasma cells before our eyes.”

According to the researchers, the positioning of the SPF structures on top of lymph nodes makes them perfectly positioned for fighting off infections – and fast.

They’re strategically placed at points where bacteria would invade, and contain all the ingredients required to keep the infection at bay.

Now we know how the body does it, we might be able to improve vaccine techniques – vaccines currently focus on making memory B cells, but this study suggests the process could be made more efficient by also looking at how they transform into plasma cells through the inner workings of an SPF.

“So this is a structure that’s been there all along, but no one’s actually seen it yet, because they haven’t had the right tools,” says Phan.

“It’s a remarkable reminder that there are still mysteries hidden within the body – even though we scientists have been looking at the body’s tissues through the microscope for over 300 years.”

The research has been published in Nature Communications.


Even the occasional drink is harmful to health, according to the largest and most detailed research carried out on the effects of alcohol, which suggests governments should think of advising people to abstain completely.

The uncompromising message comes from the authors of the Global Burden of Diseases study, a rolling project based at the University of Washington, in Seattle, which produces the most comprehensive data on the causes of illness and death in the world.

Alcohol, says their report published in the Lancet medical journal, led to 2.8 million deaths in 2016. It was the leading risk factor for premature mortality and disability in the 15 to 49 age group, accounting for 20% of deaths.

Current alcohol drinking habits pose “dire ramifications for future population health in the absence of policy action today”, says the paper. “Alcohol use contributes to health loss from many causes and exacts its toll across the lifespan, particularly among men.”

Most national guidelines suggest there are health benefits to one or two glasses of wine or beer a day, they say. “Our results show that the safest level of drinking is none.”

The study was carried out by researchers at the Institute of Health Metrics and Evaluation (IHME), who investigated levels of alcohol consumption and health effects in 195 countries between 1990 to 2016. They used data from 694 studies to work out how common drinking was and from 592 studies including 28 million people worldwide to work out the health risks.

Moderate drinking has been condoned for years on the assumption that there are some health benefits. A glass of red wine a day has long been said to be good for the heart. But although the researchers did find low levels of drinking offered some protection from heart disease, and possibly from diabetes and stroke, the benefits were far outweighed by alcohol’s harmful effects, they said.

Drinking alcohol was a big cause of cancer in the over-50s, particularly in women. Previous research has shown that one in 13 breast cancers in the UK were alcohol-related. The study found that globally, 27.1% of cancer deaths in women and 18.9% in men over 50 were linked to their drinking habits.

In younger people globally the biggest causes of death linked to alcohol were tuberculosis (1.4% of deaths), road injuries (1.2%), and self-harm (1.1%).

In the UK, the chief medical officer Sally Davies has said there is no safe level of drinking, but the guidance suggests that drinkers consume no more than 14 units a week to keep the risks low. Half a pint of average-strength lager contains one unit and a 125ml glass of wine contains around 1.5 units.

While the study shows that the increased risk of alcohol-related harm in younger people who have one drink a day is small (0.5%), it goes up incrementally with heavier drinking: to 7% among those who have two drinks a day (in line with UK guidance) and 37% for those who have five.

One in three, or 2.4 billion people around the world, drink alcohol, the study shows. A quarter of women and 39% of men drink. Denmark has the most drinkers (95.3% of women, and 97.1% of men). Pakistan has the fewest male drinkers (0.8%) and Bangladesh the fewest women (0.3%). Men in Romania and women in Ukraine drink the most (8.2 and 4.2 drinks a day respectively), while women in the UK take the eighth highest place in the female drinking league, with an average of three drinks a day.

“Alcohol poses dire ramifications for future population health in the absence of policy action today. Our results indicate that alcohol use and its harmful effects on health could become a growing challenge as countries become more developed, and enacting or maintaining strong alcohol control policies will be vital,” said the report’s senior author, Prof Emmanuela Gakidou.

“Worldwide we need to revisit alcohol control policies and health programmes, and to consider recommendations for abstaining from alcohol. These include excise taxes on alcohol, controlling the physical availability of alcohol and the hours of sale, and controlling alcohol advertising. Any of these policy actions would contribute to reductions in population-level consumption, a vital step toward decreasing the health loss associated with alcohol use.”

Dr Robyn Burton, of King’s College London, said in a commentary in the Lancet that the conclusions of the study were clear and unambiguous. “Alcohol is a colossal global health issue and small reductions in health-related harms at low levels of alcohol intake are outweighed by the increased risk of other health-related harms, including cancer,” she wrote.

“There is strong support here for the guideline published by the Chief Medical Officer of the UK who found that there is ‘no safe level of alcohol consumption’.”

Public health policy should be to prioritise measures to reduce the numbers who drink through price increases, taxation, or setting the price according to the strength of the drink (minimum unit pricing), followed by curbs on marketing and restricting the places where people can buy alcohol.

“These approaches should come as no surprise because these are also the most effective measures for curbing tobacco-related harms, another commercially mediated disease, with an increasing body of evidence showing that controlling obesity will require the same measures,” she wrote.

Ben Butler, a Drinkaware spokesperson, said: “This new study supports existing evidence about the harms associated with alcohol. Our research shows that over a quarter of UK adults typically exceed the low risk drinking guidelines and are running the risk of serious long term illnesses.”

But David Spiegelhalter, Winton professor for the public understanding of risk at the University of Cambridge, said the data showed only a very low level of harm in moderate drinkers and suggested UK guidelines were very low risk.

“Given the pleasure presumably associated with moderate drinking, claiming there is no ‘safe’ level does not seem an argument for abstention,” he said. “There is no safe level of driving, but government do not recommend that people avoid driving. Come to think of it, there is no safe level of living, but nobody would recommend abstention.”

Reprinted from The Lancet Neurology,, Trapp et al, Cortical neuronal densities and cerebral white matter demyelination in multiple sclerosis: a retrospective study, Copyright (2018), with permission from Elsevier

Bruce Trapp, Ph.D., chair of Cleveland Clinic’s Lerner Research Institute Department of Neurosciences

Cleveland Clinic researchers have discovered a new subtype of multiple sclerosis (MS), providing a better understanding of the individualized nature of the disease.

MS has long been characterized as a disease of the brain’s white matter, where immune cells destroy myelin – the fatty protective covering on nerve cells. The destruction of myelin (called demyelination) was believed to be responsible for nerve cell (neuron) death that leads to irreversible disability in patients with MS.

However, in the new findings, a research team led by Bruce Trapp, Ph.D., identified for the first time a subtype of the disease that features neuronal loss but no demyelination of the brain’s white matter. The findings, published in Lancet Neurology, could potentially lead to more personalized diagnosis and treatments.

The team’s findings support the concept that neurodegeneration and demyelination can occur independently in MS and underscore the need for more sensitive MRI imaging techniques for evaluating brain pathology in real time and monitoring treatment response in patients with the disease. This new subtype of MS, called myelocortical MS (MCMS), was indistinguishable from traditional MS on MRI. The researchers observed that in MCMS, part of the neurons become swollen and look like typical MS lesions indicative of white matter myelin loss on MRI. The disease was only diagnosed in post-mortem tissues.

“This study opens up a new arena in MS research. It is the first to provide pathological evidence that neuronal degeneration can occur without white matter myelin loss in the brains of patients with the disease,” said Trapp, chair of Cleveland Clinic’s Lerner Research Institute Department of Neurosciences. “This information highlights the need for combination therapies to stop disability progression in MS.”

In the study of brain tissue from 100 MS patients who donated their brains after death, the researchers observed that 12 brains did not have white matter demyelination. They compared microscopic tissue characteristics from the brains and spinal cords of 12 MCMS patients, 12 traditional MS patients and also individuals without neurological disease. Although both MCMS and traditional MS patients had typical MS lesions in the spinal cord and cerebral cortex, only the latter group had MS lesions in the brain white matter.

Despite having no typical MS lesions in the white matter, MCMS brains did have reduced neuronal density and cortical thickness, which are hallmarks of brain degeneration also observed in traditional MS. Contrary to previous belief, these observations show that neuronal loss can occur independently of white matter demyelination.

“The importance of this research is two-fold. The identification of this new MS subtype highlights the need to develop more sensitive strategies for properly diagnosing and understanding the pathology of MCMS,” said Daniel Ontaneda, M.D., clinical director of the brain donation program at Cleveland Clinic’s Mellen Center for Treatment and Research in MS. “We are hopeful these findings will lead to new tailored treatment strategies for patients living with different forms of MS.”

Dr. Trapp is internationally known for his work on mechanisms of neurodegeneration and repair in MS and has published more than 240 peer-reviewed articles and 40 book chapters. He also holds the Morris R. and Ruth V. Graham Endowed Chair in Biomedical Research. In 2017 he received the prestigious Outstanding Investigator award by the National Institute of Neurological Disorders and Stroke to examine the biology of MS and to seek treatments that could slow or reverse the disease.

Elephants’ secret to their low rates of cancer might be explained in part by a so-called zombie gene—one that was revived during evolution from a defunct duplicate of another gene. In the face of DNA damage, elephant cells fire up the activity of the zombie gene LIF6 to kill cells, thereby destroying any cancer-causing genetic defects, researchers reported in Cell Reports.

“From an evolutionary biology perspective, it’s completely fascinating,” Joshua Schiffman, a pediatric oncologist at the University of Utah who was not involved in the work, tells National Geographic.

The better-known LIF gene has a number of functions in mammals, including as an extracellular cytokine. In elephants, LIF is duplicated numerous times as pseudogenes, which don’t have the proper sequence to produce functioning transcripts. For the latest study, the researchers wanted to see whether the duplications might have anything to do with elephant cells’ unusual response to DNA damage: indiscriminant destruction.

The team found that one of the pseudogenes, LIF6, evolved after LIF was duplicated in a way that produces a transcript, and that the gene product is controlled by TP53, a tumor suppressor. When the researchers overexpressed LIF6 in elephant cells, the cells underwent apoptosis. The same thing happened with they introduced the gene to Chinese hamster ovary cells, indicating that LIF6 has a role in elephants’ defense against DNA damage.

More work needs to be done to determine whether the LIF6 revival is responsible for elephants’ low cancer rates. There are likely to be other contributors, says coauthor Vincent Lynch, an evolutionary biologist at the University of Chicago, in an interview with The New York Times. “There are lots of stories like LIF6 in the elephant genome, and I want to know them all.”