Monthly Archives: July 2021

Jul 01, 2021 5:30 PM

Author: Doug Dollemore

During his 17-year career with the New York Yankees, Lou Gehrig was famed for his prowess as a hitter and for his durability on the baseball field, which earned him his nickname "The Iron Horse. Then, mysteriously, in 1938, his iron body began to figuratively rust. He couldnt run, hit, or field his position as well as he once did. When doctors finally diagnosed his condition, the news was devastating.

Gehrig had amyotrophic lateral sclerosis (ALS), a rare progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord. People who have ALS gradually lose their ability to control muscle movement. Eventually, the condition, now often referred to as Lou Gehrigs disease, leads to total paralysis and death. Then, as now, there is no cure.

In the 80 years since Gehrigs death at age 37, scientists have sought to unravel what causes the disease and develop better treatments for it.

In the latest advance, University of Utah Health researchers have detected a set of genetic mutations that appear to increase a persons risk of developing ALS. They say the discovery of mutations in TP73, a gene that has never been associated with ALS before, could help scientists develop new therapies to slow or even stop the progression of the disease.

Its really a novel discovery that suggests a very different pathway for the onset of at least some cases of ALS that hasnt been explored before, says Lynn Jorde, Ph.D., chair of the Department of Human Genetics at U of U Health and the senior author of the study. From a scientific standpoint, its going to provide us with a more complete picture of what is going wrong in ALS and expand our understanding of what can be done to mitigate its devastating consequences.

The study appears in Neurology, the medical journal of the American Academy of Neurology.

"From a scientific standpoint, its going to provide us with a more complete picture of what is going wrong in ALS and expand our understanding of what can be done to mitigate its devastating consequences."

About 85% of ALS cases are sporadic, meaning that no one in a patients family has a history of the disease. However, researchers suspect that up to 61% of sporadic ALS cases are influenced by genetic factors. But detecting those factors has been challenging.

In the past, it has been difficult to determine ALS-causing genes because only recently has sequencing technology advanced enough to feasibly sequence many patients, says Kristi L. Russell, a graduate research assistant at U of U Health and lead author of the study. Additionally, many mutations in a single patient could be considered deleterious, so one must test the candidate mutations in animal models or cell culture, an incredibly time-consuming process.

For this study, Jorde, Russell, and colleagues analyzed blood samples provided by 87 people with sporadic ALS who were being treated at U of U Health. Using a technique called exome sequencing, which zeroes in on the protein-coding regions within genes, they found five people who had rare, deleterious mutations in the TP73 gene, which plays a key role in apoptosis or programmed cell death. Then, the researchers studied data from 2,900 other sporadic ALS patients from the Utah Heritage 1K Project and the ALSdb cohort. Within these groups, they identified 24 different, rare protein-coding variants in TP73.

When the researchers did a similar analysis among 324 people who did not have ALS, the patient mutations in TP73 were not present.

In subsequent laboratory studies, knocking out or disabling TP73 in zebrafish impaired the development of nerve cells in a way that mimicked what appears to occur in ALS. Like in ALS, the zebrafish had fewer motor neurons and shorter axons, nerve fibers that transmit electrical impulses from neurons to muscle cells. This shortening could impede the axons ability to transmit impulses. Shorter axons transmit these impulses far less efficiently.

During their experiments, the researchers also found evidence that mutant TP73, which normally inhibits apoptosis in motor neurons, doesnt work properly. As a result, they suspect that apoptosis is more likely to occur.

It seems that mutant TP73 disrupts apoptosis, which leads to more neuronal death, Russell says. Many biological pathways have been implicated in ALS progression, but our study highlights the underappreciated role of apoptosis in ALS pathology. Apoptosis could potentially become a new focus or target for treatment drug screens.

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Newly Discovered Genetic Mutations May Increase Risk for Lou Gehrig's Disease - University of Utah Health Sciences

An Oxford-led team, working with Cambridge and international scholars, has discovered hundreds of genetic markers driving two of life's most momentous milestones - the age at which people first have sex and become parents.

In a paper published today inNature Human Behaviour, the team linked 371 specific areas of our DNA, called genetic variants (known locations on chromosomes), 11 of which were sex-specific, to the timing of first sex and birth. These variants interact with environmental factors, such as socioeconomic status and when you were born, and are predictors of longevity and later life disease.

The researchers conducted a Genome-Wide Association Study (GWAS), a search across the entire human genome, to see if there is a relationship between reproductive behaviour and a particular genetic variant. In the largest genomic study ever conducted to date, they combined multiple data sources to examine age at first sex (N=387,338) and birth (N=542,901) in men and women. They then calculated a genetic score, with all genetic loci combined explaining around 5-6% of the variability in the average age at sexual debut or having a first child.

Professor Melinda Mills, Director of the Leverhulme Centre for Demographic Science at the University of Oxford and Nuffield College, and the study's first author says, 'Our study has discovered hundreds additional genetic markers that shape this most fundamental part of our lives and have the potential for deeper understanding of infertility, later life disease and longevity.'

The genetic signals were driven by social factors and the environment but also by reproductive biology, with findings related to follicle-stimulating hormone, implantation, infertility, and spermatid differentiation.

Professor Mills adds 'We already knew that childhood socioeconomic circumstances or level of education were important predictors of the timing of reproduction. But we were intrigued to find literally not only hundreds of new genetic variants, but also uncover a relationship with substance abuse, personality traits such as openness and self-control, ADHD and even predictive of some diseases and longevity .'

Professor Mills says, 'We demonstrated that it is a combination of genetics, social predictors and the environment that drives early or late reproductive onset. It was incredible to see that the genetics underlying early sex and fertility were related to behavioural dis-inhibition, like ADHD, but also addiction and early smoking. Or those genetically prone to postpone sex or first birth had better later life health outcomes and longevity, related to a higher socioeconomic status in during childhood.'

Genetic factors driving reproductive behaviour are strongly related to later life diseases such as Type 2 diabetes and cardiovascular disease.

'It is exciting that the genetics underlying these reproductive behaviours may help us understand later life disease.'

Professor Mills concludes, 'Starting your sexual journey early is rooted in childhood inequality but also has links with health problems, such as cervical cancer and depression. We found particularly strong links between early sexual debut, ADHD and substance abuse, such as early age at smoking. We hope our findings lead to better understanding of teenage mental and sexual health, infertility, later life disease and treatments to help.'

Reference: Mills MC, Tropf FC, Brazel DM, et al. Identification of 371 genetic variants for age at first sex and birth linked to externalising behaviour. Nature Human Behaviour. Published online July 1, 2021. doi: 10.1038/s41562-021-01135-3.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Genes Can Drive When We Choose To Have Sex, and Become Parents - Technology Networks

Researchers headed by a team at Columbia University Vagelos College of Physicians and Surgeons have linked distinct patterns of genetic mutations with obsessive-compulsive disorder (OCD) in humans. Reporting in Nature Neuroscience on their analysis of exome sequencing data from more than 1,000 individuals with OCD, the scientists say their findings support a contribution of rare damaging coding variation to OCD risk. They suggest the work confirms the validity of targeting specific genes as a potential treatment approach for OCD, and also points to new avenues of study for the commonly debilitating condition.

Senior study author David Goldstein, PhD, director of the Institute for Genomic Medicine at Columbia, and colleagues reported on their study in a paper titled, Exome sequencing in obsessive-compulsive disorder reveals a burden of rare damaging coding variants. The multi-institution collaboration also included scientists from the University of North Carolina at Chapel Hill, the David Geffen School of Medicine in Los Angeles, Harvard Medical School, and SUNY Downstate Medical Center in Brooklyn.

OCD is a neuropsychiatric condition characterized by persistent, intrusive thoughts (obsessions) and repetitive, intentional behaviors (compulsions), the authors explained. The condition, which affects 12% of the population, commonly runs in families, and genes are known to play a large role in determining who develops the disease. Evidence from family-based studies supports a genetic contribution to the disorder, the team wrote. But while strongly acting mutations have been hypothesized to exist in OCD, statistically reliable evidence has been difficult to obtain.

Goldstein stated, Many neurological diseases are influenced by strongly acting mutations which can cause disease by themselves. These mutations are individually very rare but important to find because they can provide a starting point for the development of therapeutics that target precise underlying causes of disease.

Most previous studies on the genetics of OCD have used a candidate gene approach, in which researchers focus on plausible genes that might be involved in pathogenesis and look for genetic signatures of risk. Although that approach has had some successes, it can lead to challenges in statistical interpretation and can miss unexpected genes. As a result, both funding agencies and the pharmaceutical industry increasingly focus on genome-wide analyses that can securely implicate genes in disease risk.

But as the researchers noted, Genome-wide association studies of common single-nucleotide polymorphisms (SNPs) have not found variants that were associated with OCD at the genome-wide level of statistical significance, likely owing to insufficient sample size. Goldstein further suggested, The solution to the problem is to study all the genes in the genome at the same time and ask whether any of them have significant evidence of influencing risk. That had not been done yet at scale in OCD.

In collaboration with Gerald Nestadt, MBBCh, a psychiatrist at Johns Hopkins University with access to a cohort of OCD patients, Goldsteins team combined high-throughput sequencing and computational biology techniques to identify relevant genes anywhere in the genome. The investigators looked at genes that encode protein using whole exome sequencing in 1,313 OCD patients, and compared them to similarly large control groups.

The analysis identified a strong correlation between OCD and rare mutations, particularly in a gene called SLITRK5 that had been previously linked to OCD in candidate-gene studies. SLITRK5 is a member of the SLITRK gene family, which influences excitatory and inhibitory synapse formation, the authors wrote. Interestingly, they continued, Slitrk5-knockout mice have been described as having increased OCD-like behaviors, including elevated anxiety and excessive grooming In human samples, a burden of SLITRK5 coding variants that influence synapse formation in vitro has previously been described in OCD cases relative to controls. The study also identified a specific pattern of variation in other genes. Across the exome, there was an excess of loss of function (LoF) variation specifically within genes that are LoF-intolerant. As Goldstein further stated, When you look at genes that do not tolerate variation in the human population, those are the genes most likely to cause disease, and with OCD, we see an overall increased burden of damaging mutations in those genes compared to controls. Thats telling us that there are more OCD genes to be found and where to find them.

The authors concluded, This study is, to our knowledge, the most comprehensive cataloguing of contributions to OCD risk from rare damaging coding SNVs [single nucleotide variants] and indels thus far. Its findings suggest that, like the genetic architecture of other neuropsychiatric disorders, OCD involves contributions to overall risk from these variants.

Goldstein expects that the new data on SLITRK5 will encourage pharmaceutical companies and translational researchers to develop drugs that target this gene. OCD is a disabling disorder that is twice as common as schizophrenia, said H. Blair Simpson, MD, PhD, professor of psychiatry at Columbia University Vagelos College of Physicians and Surgeons and director of the Center for OCD & Related Disorders at New York State Psychiatric Institute, who was not involved with the new study. Two available treatments, serotonin reuptake inhibiting drugs and cognitive-behavioral therapy, are highly effective, Simpson noted, but only work on about half of patients. Thus, these genetic findings are very exciting; they indicate that the promise of precision medicine could include OCD, ultimately transforming how we diagnose and treat this disorder.

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Patterns of Genetic Mutations Linked with Obsessive-Compulsive Disorder in Humans - Genetic Engineering & Biotechnology News

In the first analysis of its kind, researchers at Columbia University Vagelos College of Physicians and Surgeons and several other institutions have linked distinct patterns of genetic mutations with obsessive-compulsive disorder (OCD) in humans.

The work, in Nature Neuroscience, confirms the validity of targeting specific genes to develop new OCD treatments and points toward novel avenues for studying this often debilitating condition.

OCD, which affects 1% to 2% of the population, often runs in families and genes are known to play a large role in determining who develops the disease. However, the identity of many OCD genes remains unknown.

Many neurological diseases are influenced by strongly acting mutations which can cause disease by themselves, saysDavid Goldstein, PhD, director of the Institute for Genomic Medicine at Columbia and a senior author on the new paper. These mutations are individually very rare but important to find because they can provide a starting point for the development of therapeutics that target precise underlying causes of disease.

Although strongly acting mutations have been hypothesized to exist in OCD, statistically reliable evidence has been difficult to obtain.

Most previous studies on the genetics of OCD have used a candidate gene approach, in which researchers focus on plausible genes that might be involved in pathogenesis and look for genetic signatures of risk. Although that approach has had some successes, it can lead to challenges in statistical interpretation and can miss unexpected genes. As a result, both funding agencies and the pharmaceutical industry increasingly focus on genome-wide analyses that can securely implicate genes in disease risk.

The solution to the problem is to study all the genes in the genome at the same time and ask whether any of them have significant evidence of influencing risk. That had not been done yet at scale in OCD, says Goldstein.

In collaboration with Gerald Nestadt, MBBCh, a psychiatrist at Johns Hopkins University with access to a cohort of OCD patients, Goldsteins team took this genome wide approach, which uses high-throughput sequencing and computational biology techniques to identify relevant genes anywhere in the genome.

The investigators looked at genes that encode protein using whole exome sequencing in more than 1,300 OCD patients and compared them to similarly large control groups. The multi-institution collaboration also included scientists from the University of North Carolina at Chapel Hill, the David Geffen School of Medicine in Los Angeles, Harvard Medical School, and SUNY Downstate Medical Center in Brooklyn.

Goldstein expects that the new data on SLITRK5 will encourage pharmaceutical companies and translational researchers to develop drugs that target this gene.

The study also identified a specific pattern of variation in other genes. When you look at genes that do not tolerate variation in the human population, those are the genes most likely to cause disease, and with OCD, we see an overall increased burden of damaging mutations in those genes compared to controls, Goldstein says. Thats telling us that there are more OCD genes to be found and where to find them.

For patients suffering from OCD and their doctors, new treatments cant come too soon. OCD causes uncontrollable, recurring thought patterns and behaviors that interfere with patients daily lives.

OCD is a disabling disorder that is twice as common as schizophrenia, says H. Blair Simpson, MD, PhD, professor of psychiatry at Columbia University Vagelos College of Physicians and Surgeons and director of the Center for OCD & Related Disorders at New York State Psychiatric Institute, who was not involved with the new study.

Two available treatments, serotonin reuptake inhibiting drugs and cognitive-behavioral therapy, are highly effective, Simpson adds, but only work on about half of patients. Thus, these genetic findings are very exciting; they indicate that the promise of precision medicine could include OCD, ultimately transforming how we diagnose and treat this disorder.

Reference: Halvorsen M, Samuels J, Wang Y, et al. Exome sequencing in obsessivecompulsive disorder reveals a burden of rare damaging coding variants. Nat Neurosci. 2021. doi: 10.1038/s41593-021-00876-8.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Genetic Mutations Linked With OCD in Humans - Technology Networks

The same journalist and I have been verifying this opinion for over eight years now indeed, observing the development of a juvenile representative of the Homo sapiens species is a continuous, fascinating adventure.

It's a fact that evolutionary success is determined not by the length of adult individuals' lives, but by the number of their offspring that carry their genes into subsequent generations. More precisely, it's not about the number of one's children, but one's grandchildren: the children need to survive and pass on their genes. Of course, in order to have children, one must beget them, or at least somehow initiate the development of the egg, as it happens in parthenogenetic species, where females don't bother with guys at all, or only rarely. But I've already written before about various original methods of completing that first stage, so let's focus on what happens later.

Ecology differentiates two strategies of reproduction: 'r-selection' and 'K-selection'. The symbols are taken from a complicated formula illustrating population dynamics developed in 1838, which systematized our thinking about animal success for the rest of the 19th century and for almost all of the 20th century. It was developed by Pierre Franois Verhulst (18041849), and its simplified version is as follows: dN/dt = rN (1 N/K), where N is the population, r is its maximum growth rate, K is the carrying capacity of the local environment, and dN/dt is the rate of change of the population with time. According to this model, species that engage in r-selection produce as much offspring as quickly as possible, while K-selection involves an investment in quality rather than quantity. So we either have masses of children that we're not too worried about, hoping that things will work out and some of them will survive; or we have few, but we invest a lot in them and we try to make sure that they do as well as possible. Of course, as is often the case, in nature it's more of a continuum, where not only different species, but also different individuals from the same species, function somewhere between these extremes and we can only say that one is 'more r' or 'more K'.

For example, guppies small fish from South and Central America, popular with both aquarists and evolutionary biologists are very flexible in this regard. Researchers have been studying them for years in Trinidadian streams and it turns out that their strategies vary widely depending on the presence of predators, sometimes within the space of a few metres. In the upper reaches of the streams, where rocks make it impossible for bigger fish to get through, guppies have fewer, but larger and better-fed young, so they're 'more K', and their offspring grow up peacefully in calm waters. Below the rocks (sometimes literally one boulder is all it takes) they choose a strategy more closely aligned with r-selection their offspring are smaller, but they're much more numerous, because in the face of the constant risk of being eaten it makes sense to have as many as possible. So, although science is currently leaving this classic model behind, speaking more often about the diversity of survival strategies, my opinion is that with some reservations these two letters make it easier for us to describe a complex reality.

Still, no matter how much offspring there is to be, they need to be brought into the world somehow. Here, there are fundamentally two methods. You can lay an egg with a yolk (the evolutionary equivalent of a packed lunch) from which after a while, with more or less assistance from the parents, your kids will hatch; or you can nourish the offspring within your own body and give birth to them ready-made. It's an easy guess that apart from oviparity and viviparity there's also a third option: ovoviviparity. It refers to embryos that develop in eggs that hatch while still in the mother's body, which the young leave later.

Let's start ab ovo. The egg must be encased in something, so that it can protect the embryos at least a little from outside danger. Species that lay their eggs in water usually don't have to worry that they'll dry out, so for them a jelly-like membrane is usually enough; it means the contents of the egg stay where they should, instead of sloshing around. But if you live on land, you must like many insects and arachnids, and all reptiles and birds, as well as mammals such as the platypus and the echidna invest in something more watertight. The hard shell of a bird's egg also protects it from at least some predators. For example, the shell of an ostrich egg incidentally, the largest single cell in the world is so thick and strong that even lions have trouble breaking it.

Photo by Anna Sjblom on Unsplash

Still, whatever the eggs are encased in, they all have a better chance of surviving if someone looks after them. We automatically associate incubating eggs with birds; indeed, they either take care of their clutch themselves or, like cuckoos, frame someone else into doing it. But other animals also provide many examples of parental dedication. Female octopuses spend the last weeks of their lives defending their eggs, tucked away in some underwater nook, oxygenating them and cleansing away algae and parasites. This work uses up all the time and energy they've got left after the enormous effort of producing and laying the eggs in a suitable place. When the young octopuses finally hatch, their mum is either already dead or about to die. Although this strategy seems to suit cephalopods, we owe our current position in the world to it I suspect that if a mother octopus could pass her knowledge and experience to her offspring, Earth would be a very different place. As it is, despite their astonishing intelligence, each octopus must re-invent the wheel. Considering that their intelligence precedes ours by a few million years, I really think that if they could accumulate experience from generation to generation, I'd be writing this text for an eight-legged editor-in-chief, had she even been interested in the opinion of an organism as inferior as a human.

Although the sacrifice of the cephalopod mum is impressive, some invertebrates go further. Perhaps the most extreme form of parental devotion is matriphagy, or the consumption of the mother by her newly-hatched offspring. This phenomenon can be observed in some arachnid species: after laying the eggs, the female starts to dissolve the tissues of her body with digestive juices, so that when the adorable spider babies hatch, their mother is nothing more than an eight-legged chitin container filled with nutritious juice. The tots just need to bite through her skin and they can lap it up. Among insects, apart from the obvious examples of the Hymenoptera (i.e. ants, wasps and bees) and termites, earwigs provide another example of exemplary parental care. The Japanese species Anechura harmandi is the only insect known to science in which the mother also dies before the young hatch, to become their first meal. Even the common earwig is no stranger to motherly sacrifice. The females of these rather unpopular fearless vanquishers of aphids and silverfish frequently gather into groups to care for their clutches together, and then to feed their young and bravely defend them from predators.

Laying eggs has its obvious advantages. If they require no care, you can not only produce many, but also expect that they will spread around the world on their own. But carrying their offspring in their own bodies makes it easier for parents to provide suitable conditions for development. No wonder, then, that some animals (including many species of shark and the common European adder) have chosen the compromise of ovoviviparity during their evolution. In others like in the viviparous lizard one or the other method of reproduction dominates depending on environmental conditions. In Southern Europe these lizards, like most lizard species, lay eggs. But in cooler areas the females give birth to their young. Thanks to this flexible strategy, they can live in environments that are inaccessible to many other species, like high up in the mountains and the far north of Europe. It is the only reptile on our continent that also lives beyond the polar circle, although vipers the northernmost of our snakes reach almost as far north as that.

Another interesting issue is laying your eggs in someone else's body, although I'm not sure if that still counts as ovoviviparity. The most banal and drastic example are the many species of parasitoids animals that exploit their host completely, living in it for a time, before killing it like the Alien from the famous science fiction film. Many wasps paralyse their victim (usually a caterpillar or a spider) and lay their eggs in that living larder; the larvae will later gradually bite their way out of it. But laying eggs into the body of one's own partner is even more interesting.

This is what happens in the Hippocampus, or the slowly moving fish known as seahorses. After their mating dance and successful consummation of the relationship, the female lays the fertilized eggs into a special pouch on the male's front. From then on, they will be in his care, so that one day he can give birth to hundreds of miniature seahorses, which he will still take care of after the birth.

But since early childhood, I have been fascinated by another organism. The common Suriname toad a tailless amphibian (i.e. frog-adjacent) from the northern part of South America with the charming Latin name Pipa pipa appeared in my life in the form of an illustration in an ancient animal atlas, and it immediately hopped onto the pedestal as one of my favourite species of all times. Just after the female lays the eggs, the male gathers them up and distributes them evenly on her sticky back. Her skin grows spongy, and the eggs sink into it and develop relatively safely; after a time, fully formed little frogs leave her back. It is undoubtedly one of the most interesting births in nature.

If the young isn't separated from its mother's organism by the egg shell, she usually nourishes it via a placenta. This is, of course, the case in a substantial majority of mammals, but not exclusively. The placenta can also be found in some sharks and lizards, but true viviparity has evolved independently at least 150 times and occurs in many species of fish, amphibians, insects and arachnids. One of these unexpectedly caring parents is the infamous tsetse fly: the female flies around for nine months with a single, increasingly large larva in her abdomen, feeding it with a nutritious milky liquid. A more macabre version of feeding one's young can be observed in some Gymnophiona from the family of common caecilians. Their embryos have special teeth that allow them to feed on the epithelium of the mother's oviduct. After they're born, young common caecilians switch over to the female's outer epithelium and literally flay her, although fortunately she regenerates quickly.

After leaving the mother's body one way or another many young animals still need constant care. Because the physical connection is no longer there, persuading the parents to continue to provide food and shelter requires initiating a psychological bond. The parents must like their newly born or hatched children to keep taking care of them.

And so evolution has equipped young animals with a whole arsenal of signals that leave their carers helpless. In birds, it's frequently a lurid colouration of the inside of the beak and the area around it, visible when it is fully open. Adult birds find this irresistible and stuff food down the open, begging mouth, even if it doesn't belong to their children but, for example, to a fish taking advantage of the situation. It is due to our own primitive instincts that most of us also feel tenderness and an urgent need to take care of young animals (or ones that look young). What's more, the recipients of that care don't even need to be cute, pretty bunnies I still remember how touched I was when, as a student, I discovered a wryneck nest in one of the nest boxes I was checking. The chicks of this woodpecker, with their thin, twisty necks and flat heads, look like mould-infested hallucinogenic mushrooms and they're certainly not pretty, but it works. Their relatively big eyes and squeaky sounds are all it takes. Of course, if the animal meets our criteria of beauty, the effect is even stronger. Cats blatantly exploit this the charm of their small faces, large eyes and the meowing that emulates the voice of a human baby turns out to be so strong that even my geologist friend is unable to resist them. Although due to his profession he is used to communing with nature through the means of a hammer, he can't stop himself and constantly regales everyone with photos of his feline charges on social media.

There's no doubt, however, that in animals such as birds and mammals it's not only the case of a simple reflex. For some time now, researchers have been claiming more and more boldly that other animals also experience feelings and emotions, like fear, anger, boredom and love. And love for one's offspring is probably the easiest to observe. It is the simplest explanation for such dramatic examples as the behaviour of a killer whale called Tahlequah who, two years ago, carried the body of her dead child with her for 17 days. Parental love can also be the explanation because there is no other for more prosaic and happy examples of behaviour, such as the fact that I'm about to walk my daughter to school, even though I've spent all night writing this text.

Translated from the Polish by Marta Dziurosz.

Reprinted with permission of Przekrj. Read the original article.

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Penn scientists correct genetic blindness with single injection into the eye - Big Think