Neuroscience

Psychedelics should be used to treat depression – The Ecologist

Psychedelic drugs such as LSD and magic mushrooms should be used to treat depression and alcoholism, a new study has claimed.

According to the report, published in the scientific journal Cell, such psychedelics are an effective tool against a number of mental health conditions but have become an unfortunate victim of the global war on drugs.

The now-banned drugs were regularly used as treatments around the world until about 50 years ago.

Neuroplastic

Now, the government's former chief drugs adviser Professor David Nutt is among the team of scientists behind the study who are calling for "the resurrection of research into the neuroscience and therapeutic application of psychedelics".

"It (would rectify) decades of global research paralysis that emerged as collateral damage from the war on drugs," they write.

The study claims that brain imaging has revealed the "powerful neuroplastic changes" of psychedelics can have numerous long-term benefits for people suffering from a variety of mental health conditions.

"What is now needed is a combined, multi-level, multidisciplinary program of research into the mechanisms underpinning these findings," the report says.

This Author

Brendan Montague is editor of The Ecologist.

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Biochemistry

Former University of Birmingham Professor Michael Wakelam dies after suspected coronavirus infection – University of Birmingham

Mike Wakelam served as Professor of Molecular Pharmacology in the Institute of Cancer Studies from 1993-2007

The University of Birmingham was devastated to hear the news of the death of Professor Michael Wakelam, a former member of staff and an alumnusof the College of Medical and Dental Sciences.

Michael Wakelam died from respiratory complications arising from a suspected Covid-19 infection.

Michael Wakelam served as Professor of Molecular Pharmacology in the Institute of Cancer Studies from 1993-2007 before leaving to become director of the Babraham Institute, Cambridge.

Micheal's links to the University of Birmingham go beyond his teaching and research as he had also obtained his BSc in Medical Biochemistry (1977) and PhD in Biochemistry (1980) from Birmingham as well. Before taking up his post in 1993 at the University, Michael had pursued post-doctoral research at the University of Konstanz in Germany and Imperial College London as a Beit Memorial Fellow. In 1985 he was appointed as a lecturer in Biochemistry at the University of Glasgow.

Michael Wakelam also was a Honorary Professor at the University of Birmingham, as well as a Honorary Professor of Lipid Signalling in the Cambridge University Clinical School. He also served as a visiting Professor at Kings College London and as a Fellow of the Royal Society of Biology and a member of the Academia Europaea. In 2018 Mike received the Morton Lectureship from the Biochemical Society.

Paying tribute to Michael Wakeham, Professor David Adams, Pro-Vice-Chancellor and the Head of College of Medical and Dental Sciences said:

"The College of Medical and Dental Sciences was devastated to hear last night about the death of Professor Michael Wakelam from a suspected Covid-19 infection. Mikes links to Birmingham go even further back as he was an undergraduate and then PhD student in Biochemistry here. Those of you who knew Mike will remember him not only as a superb scientist but also as a warm, supportive and highly collaborative colleague, Mike will be greatly missed. Our thoughts go out to his wife Jane and sons Alex and Patrick."

Michael Wakelam had over twenty years research experience in the area of cell signalling and communication; a major focus of his research was upon the use and development of advanced lipidomics methodologies in determining the functions of individual lipid molecular species in the regulation of signalling pathways in normal and cancer cells and in inflammatory responses.

Michael Wakelam is survived by his wife Jane and their two sons Alex and Patrick.

For more information or interviews, please contact:Hasan Salim Patel, Communications Manager (Arts, Law and Social Sciences) or contact the press office out of hours on +44 (0)7789 921 165.

The University of Birmingham is ranked amongst the worlds top 100 institutions. Its work brings people from across the world to Birmingham, including researchers, teachers and more than 6,500 international students from over 150 countries.

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Former University of Birmingham Professor Michael Wakelam dies after suspected coronavirus infection - University of Birmingham

Biochemistry

To divide or not to divide? The mother cell may decide – CU Boulder Today

When do cells decide to divide? For 40 years, the textbook answer has been that this decision occurs in the first phase of a cells existence right after a mother cell divides to become daughter cells.

But researchers at CU Boulder have found that its actually the mother cell that determines if its daughter cells will divide. The finding, explained in a new study out today in Science, sheds new light on the cell cycle using modern imaging technologies, and could have implications for cancer drug therapy treatments.

We see something different than what's in the textbooks, said Sabrina Spencer, senior author of the paper and assistant professor of biochemistry.

Cells choose to divide based on the amount of mitogens, or growth factors, they sense in their environment. The availability of mitogens drives the signal to proliferate: duplicate cellular contents and divide into two daughter cells. This is all part of the cell cycle.

Cancer cells can enter the cell cycle even if growth factors aren't there, said Spencer. Thats part of why they proliferate so much the cell cycle becomes dysregulated and growth continues unchecked.

Sabrina Spencer points to a specific cell in an image on a screen, which contains a population of cells expressing fluorescent reporters. (Credit: BioFrontiers Institute, CU Boulder)

Better understanding of why and when cells choose to proliferate, could help scientists tailor or expand the timing of cancer drug therapies.

In their experiments, the researchers found that rather than daughter cells deciding on their own whether to divide, they committed to another cell cycle or not immediately after division of the mother cell. This implies the decision was made in the previous cell cycle, because the daughter cells were already born on one path or another, according to Spencer.

That got us thinking that maybe all the sensing of the environment is actually happening in the mother cell cycle, said Spencer.

Previous textbook experiments had to first remove all growth factors in order to synchronize the cells cycling, which perturbs cell cycle behavior. But this new research used time lapse microscopy and cell tracking technologies, which allowed the scientists to film cells doing their own thing, on their own time.Doing the experiment this way led to very different results, said Spencer.

The researchers tracked thousands of cells across 48 hours, using computational cell tracking which can track the same cell through hundreds of sequential images.

Even 10 years ago, very few labs could track cells even for a couple of hours, said Spencer.

A mother cell divides into two daughter cells, and the daughter cell is trying to decide if it is going to divide again. The answer is that it depends on the mother cells history of growth factor signaling. (Credit: Sabrina Spencer)

When do cells care about mitogen (growth factors)? In the textbook model, researchers found that the daughter cell cared in the first phase of the cell cycle about mitogen. From this new research, CU Boulder scientists found that cells are actually sensing mitogen during the entirely of the mother cell cycle. (Credit: Sabrina Spencer)

Their next question was: when in the mother cell cycle does a cell decide if its daughter cells will divide?

To answer this, the researchers removed and replaced the growth factors which give the signal for the cell to divide for several hours at different phases in the mother cell cycle.

They found that the longer these growth factors were removed in the mother cell, the less likely the daughter cells were to divide. If the growth factors were removed for more than nine hours, none of the daughter cells ended up dividing.

We found that no matter when you blocked this signaling, cells can sense it, said Mingwei Min, first author and postdoctoral researcher in the Department of Biochemistry and BioFrontiers Institute. And not only can they sense it, they can remember that information for many hours, all the way through to the daughter cell cycle.

If cells are continually sensing growth factor signaling as this new paper found instead of only in the first phase of the daughter cycle, cancer drugs may have a longer window than previously believed to provide therapeutic effects.

But how are cells remembering the availability of growth factors? The key lies in a protein known as Cyclin D.

Normally, Cyclin D rises up in the second half of the cell cycle in the mother cell. But when growth factors were removed and replaced in the experiment, there was less Cyclin D at the end of the mother cell cycle, the study found.

And without as much Cyclin D, the daughter cells have less of the thing they need to be able to divide.

The fact that cells can store memory or integrate past history of growth factor availability is a new finding, said Spencer. The combination of fluorescent sensor design, long-term time-lapse microscopy, and cell tracking is really our forte that enabled this discovery.

Additional authors on this paper include Yao Rong and Chengzhe Tian of the Department of Biochemistry and the BioFrontiers Institute at CU Boulder.

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Biochemistry

Letter to the Editor: Let there be music – Mount Desert Islander

To the Editor:

All acrossthe world, people are turning to music to help them cope and connect with others during the COVID-19 pandemic. First, we saw a plethora of handwashing songs and parodies. Next came the viral videos of people in Italy singing to each other from their balconies. The Facebook group, Quarantine Karaoke, has over 400,000 followers. Musicians are posting live concerts from home and choirs are sharing virtual group songs.

So many of us, unable to connect with each other in physical space, are doing so through music. It makes sense. Coronavirus fears have us feeling anxious, isolated and perhaps even depressed. We seem to intrinsically know that music can help us, in concrete and specific ways, withall ofthese feelings.

Making music encourages group cohesion and bonding. To music with others, people need to work together in a cooperative, synchronized manner. Research shows that when we make music together, people feel more bonded, more trusting and may even start tosynchronizeheartbeats.

Music also has a direct impact on our physiology and biochemistry. Making music reduces levels of the stress hormone cortisol and modulates levels of dopamine and serotonin, all which help improve mood.

One thing that excites me about the musical explosion happening right now is that music is being made byeveryone. Not just the professionals, but everyone. This is the way that music once was. Music was shared around the piano, in the legion hall, across the fire and on the front porch. Singing once was a part of everyday life and now, perhaps it is again.

So please, keep the music going. And when this current crisis passes, remember how important music was in helping us get through this. Remember it the next time your local school system wants to cut music programs from the budget, or community arts organizations come asking for donations. Professional musicians, music therapists, teachers, and community music groups are being financially devastated by the loss of paid work. Yet, the music goes on. Because what else can we do? We are human beings, we will persevere, and there will be music.

Carla Tanguay

Mount Desert

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Letter to the Editor: Let there be music - Mount Desert Islander

Biochemistry

Artificial proteins that function as molecular logic gates – Tech Explorist

Scientists at the University of Washington School of Medicine have devised artificial proteins that can regulate gene expression inside human T-cells. Whats interesting, these proteins can function as molecular logic gates, tools are used to program the behavior of more complex systems.

Senior author David Baker, professor of biochemistry at the UW School of Medicine and director of the Institute for Protein Design, said,Bioengineers have made logic gates out of DNA, RNA and modified natural proteins before, but these are far from ideal. Our logic gates built from de novo designed proteins are more modular and versatile, and can be used in a wide range of biomedical applications.

Whether electronic or biological, logic gates sense and respond to signals in predetermined ways. One of the simplest is the AND gate; it produces output only when one input AND another are present.

For example, when typing on a keyboard, pressing the Shift key AND the A key produces an uppercase letter A. Logic gates made from biological parts aim to bring this level of control into bioengineered systems.

With the right gates operating inside living cells, inputs such as the presence of two different moleculesor one and not the othercan cause a cell to produce a specific output, such as activating or suppressing a gene.

Lead author Zibo Chen, a recent UW graduate student, said,The whole Apollo 11 Guidance Computer was built from electronic NOR gates. We succeeded in making protein-based NOR gates. They are not as complicated as NASAs guidance computers, but are a key step toward programming complex biological circuits from scratch.

Enlisting a patients immune in the battle against cancer growth has worked for specific types of the disease. In any case, focusing on strong tumors with this so-called CAR-T cell therapy approach has demonstrated challenging.

Scientists think part of the reason has to do with T cell exhaustion. Genetically altered T cells can fight for only so long before they stop working. There may be a way around this. With protein logic gates that respond to exhaustion signals, the team from UW Medicine hopes to prolong the activity of CAR T cells.

Chen said,Longer-lived T cells that are better programmed for each patient would mean more effective personalized medicine.

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Genetics

Genes and genetics explained – Better Health Channel

Your chromosomes contain the blueprint for your body your genes. Almost every cell in the human body contains a copy of this blueprint, mostly stored inside a special sac within the cell called the nucleus. Chromosomes are long strands of a chemical substance called deoxyribonucleic acid (DNA).

A DNA strand looks like a twisted ladder. The genes are like a series of letters strung along each edge. These letters are used like an instruction book. The letter sequence of each gene contains information on building specific molecules (such as proteins or hormones both essential to the growth and maintenance of the human body).

Although every cell has two copies of each gene, each cell needs only certain genes to be switched on in order to perform its particular functions. The unnecessary genes are switched off.

Sometimes, a gene contains a change that disrupts the genes instructions. A change in a gene can occur spontaneously (no known cause) or it can be inherited. Changes in the coding that makes a gene function can lead to a wide range of conditions.

Humans typically have 46 chromosomes in each cell of their body, made up of 22 paired chromosomes and two sex chromosomes. These chromosomes contain between 20,000 and 25,000 genes. New genes are being identified all the time.

The paired chromosomes are numbered from 1 to 22 according to size. (Chromosome number 1 is the biggest.) These non-sex chromosomes are called autosomes.

People usually have two copies of each chromosome. One copy is inherited from their mother (via the egg) and the other from their father (via the sperm). A sperm and an egg each contain one set of 23 chromosomes. When the sperm fertilises the egg, two copies of each chromosome are present (and therefore two copies of each gene), and so an embryo forms.

The chromosomes that determine the sex of the baby (X and Y chromosomes) are called sex chromosomes. Typically, the mothers egg contributes an X chromosome, and the fathers sperm provides either an X or a Y chromosome. A person with an XX pairing of sex chromosomes is biologically female, while a person with an XY pairing is biologically male.

As well as determining sex, the sex chromosomes carry genes that control other body functions. There are many genes located on the X chromosome, but only a few on the Y chromosome. Genes that are on the X chromosome are said to be X-linked. Genes that are on the Y chromosome are said to be Y-linked.

Parents pass on traits or characteristics, such as eye colour and blood type, to their children through their genes. Some health conditions and diseases can be passed on genetically too.

Sometimes, one characteristic has many different forms. For example, blood type can be A, B, AB or O. Changes (or variations) in the gene for that characteristic cause these different forms.

Each variation of a gene is called an allele (pronounced AL-eel). These two copies of the gene contained in your chromosomes influence the way your cells work.

The two alleles in a gene pair are inherited, one from each parent. Alleles interact with each other in different ways. These are called inheritance patterns. Examples of inheritance patterns include:

The most common interaction between alleles is a dominant/recessive relationship. An allele of a gene is said to be dominant when it effectively overrules the other (recessive) allele.

Eye colour and blood groups are both examples of dominant/recessive gene relationships.

The allele for brown eyes (B) is dominant over the allele for blue eyes (b). So, if you have one allele for brown eyes and one allele for blue eyes (Bb), your eyes will be brown. (This is also the case if you have two alleles for brown eyes, BB.) However, if both alleles are for the recessive trait (in this case, blue eyes, bb) you will inherit blue eyes.

For blood groups, the alleles are A, B and O. The A allele is dominant over the O allele. So, a person with one A allele and one O allele (AO) has blood group A. Blood group A is said to have a dominant inheritance pattern over blood group O.

If a mother has the alleles A and O (AO), her blood group will be A because the A allele is dominant. If the father has two O alleles (OO), he has the blood group O. For each child that couple has, each parent will pass on one or the other of those two alleles. This is shown in figure 1. This means that each one of their children has a 50 per cent chance of having blood group A (AO) and a 50 per cent chance of having blood group O (OO), depending on which alleles they inherit.

Figure 1 -Fathers blood group(OO, group O)

AO

(group A)

AO

(group A)

The combination of alleles that you have is called your genotype (e.g. AO). The observable trait that you have in this case blood group A is your phenotype.

If a person has one changed (q) and one unchanged (Q) copy of a gene, and they do not have the condition associated with that gene change, they are said to be a carrier of that condition. The condition is said to have a recessive inheritance pattern it is not expressed if there is a functioning copy of the gene present.

If two people are carriers (Qq) of the same recessive genetic condition, there is a 25 per cent (or one in four) chance that they may both pass the changed copy of the gene on to their child (qq, see figure 2.) As the child then does not have an unchanged, fully functioning copy of the gene, they will develop the condition.

There is also a 25 per cent chance that each child of the same parents may be unaffected, and a 50 per cent chance that they may be carriers of the condition.

Figure 2 -Father (carrier)

QQ(unaffected)

Qq(carrier)

Recessive genetic conditions are more likely to arise if two parents are related, although they are still quite rare. Examples of autosomal recessive genetic conditions include cystic fibrosisand phenylketonuria (PKU).

Not all genes are either dominant or recessive. Sometimes, each allele in the gene pair carries equal weight and will show up as a combined physical characteristic. For example, with blood groups, the A allele is as strong as the B allele. The A and B alleles are said to be co-dominant. Someone with one copy of A and one copy of B has the blood group AB.

The inheritance pattern of children from parents with blood groups B (BO) and A (AO) is given in figure 3.

Each one of their children has a 25 per cent chance of having blood group AB (AB), A (AO), B (BO) or O (OO), depending on which alleles they inherit.

Figure 3 -Fathers blood group -(group B)

AB

(group AB)

AO

(group A)

A cell reproduces by copying its genetic information then splitting in half, forming two individual cells. Occasionally, an alteration occurs in this process, causing a genetic change.

When this happens, chemical messages sent to the cell may also change. This spontaneous genetic change can cause issues in the way the persons body functions.

Sperm and egg cells are known as germ cells. Every other cell in the body is called somatic (meaning relating to the body).

If a change in a gene happens spontaneously in a persons somatic cells, they may develop the condition related to that gene change, but wont pass it on to their children. For example, skin cancer can be caused by a build-up of spontaneous changes in genes in the skin cells caused by damage from UV radiation. Other causes of spontaneous gene changes in somatic cells include exposure to chemicals and cigarette smoke. However, if the gene change occurs in a persons germ cells, that persons children have a chance of inheriting the altered gene.

About half of the Australian population will be affected at some point in their life by a condition that is at least partly genetic in origin. Scientists estimate that more than 10,000 conditions are caused by changes in single genes.

The three ways in which genetic conditions can arise are:

Having a genetic susceptibility to a condition does not mean that you will develop the condition. It means that you are at increased risk of developing it if certain environmental factors, such as diet or exposure to chemicals, trigger its onset. If these triggering conditions do not occur, you may never develop the condition.

Some types of cancer are triggered by environmental factors such as diet and lifestyle. For example, prolonged exposure to the sun is linked to melanoma. Avoiding such triggers means significantly reducing the risks.

Related parents are more likely than unrelated parents to have children with health problems or genetic conditions. This is because the two parents share one or more common ancestors and so carry some of the same genetic material. If both partners carry the same inherited gene change, their children are more likely to have a genetic condition.

Related couples are recommended to seek advice from a clinical genetics service if their family has a history of a genetic condition.

If a family member has been diagnosed with a genetic condition, or if you know that a genetic condition runs in your family, it can be helpful to speak to a genetic counsellor.Genetic counsellors are health professionals qualified in both counselling and genetics. As well as providing emotional support, they can help you to understand a genetic condition and what causes it, how it is inherited (if it is), and what a diagnosis means for you and your family.

Genetic counsellors are trained to provide information and support that is sensitive to your family circumstances, culture and beliefs.

Genetic services in Victoria provide genetic consultation, counselling, testing and diagnostic services for children, adults, families, and prospective parents. They also provide referral to community resources, including support groups, if needed.

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Genetics

Unlocking the Genetics of Autism Spectrum Disorder – TMC News – Texas Medical Center News

Cason McKee was diagnosed with autism when he was 3 years old.

Both of his parents worked with autistic children in the Texas school system, so they saw it coming.

Early on, when we first started noticing a difference in him, he was a typical 18-month old, said Shannon McKee, Casons mother. But between 18 months and 2 years, he started to lose his language and his interest in language. It happened gradually.

At Casons second birthday party, McKee realized that her son wasnt engaging with his friends. He doesnt even carethat his friends are here, she thought.

A light bulb went off in my head, she said.

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Casons diagnosis of ASD (autism spectrum disorder) unleashed a host of questions for Shannon and Michael McKee, who began searching for the best therapies and pro- grams for their son. Once they got a grasp on their own situation, it became increasingly important for them to help other families who had received an ASD diagnosis. One of the best ways to do that, they realized, was to participate in research that could unlock some of the genetic mysteries surrounding the disorder, which affects communication and social interaction.

In 2016, the McKees were among the first families to enroll in the national SPARK for Autism study, a landmark project that aims to accelerate the pace of autism research and answer myriad genetic questions about the disorder.

More specifically, that 50,000 actually refers to triosto an individual with autism and both biological parents, Kochel explained. To date, SPARK has enrolled close to 23,000 families in a database that allows investigators to search for and identify genetic trends and similarities.

Its open to everyone, Kochel said. Basically, families enroll online. It takes about 20 to 30 minutes. They have the option to consent to providing a genetic sample.

For families who consent, a saliva kit is mailed to their home, with instructions for its use and return. Families also consent to whether or not they want to see the results of a genetic finding, if one is made.

Today, there are over 1,000 genes that have been associated with autism, and part of what SPARK is doing is to help identify more genetic causes of autism, Kochel said. We do know that autism is largely caused by genetic factors, yet when you go to get a clinical genetic test today, only a fraction of kids come back with a finding. But we still believe that theres more there, genetically, and were look- ing for it. Its just going to take some time.

SPARK hopes to identify small groups of people diagnosed with ASD who have the same genetic differencesdifferences researchers didnt know about before.

The study is a way for us to help identify those people and get them together and think about what would be valuable to learn about this particular group, Kochel said. We call it a genet- ics first approach. We might then have next-step studies that would convene those folks and say: You all have the same genetic difference. Can we work with you to see what else is similar with you? It might be certain medical conditions or other psychiatric diagnoses, things like that.

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Genetics

Study Probes Interaction of Genetics and Neural Wiring in ADHD – PsychCentral.com

A new study comparing genetics and the neural wiring of the brain suggests a diagnosis of attention-deficit/hyperactivity disorder (ADHD) results from a combination of factors. Investigators discovered that it takes many common genetic variations combining together in one individual to increase risk substantially.

At the same time, neuroimaging (MRI) experts have found differences in how the brains of people diagnosed with ADHD are functionally connected. However, its unclear how genetic risk might be directly related to altered brain circuitry in individuals diagnosed with ADHD.

In the new study, researchers focused their imaging analyses on selected brain regions, looking specifically at the communication between those regions and the rest of the brain in children with the diagnosis.

They discovered that one brain regions connectivity was linked to a higher risk of ADHD. However, a second, different part of the brain seemed to compensate for genetic effects and reduce the chances of an ADHD diagnosis.

The authors believe this research will lead to a better understanding of how genetic risk factors alter different parts of the brain to change behaviors and why some people at higher genetic risk do not exhibit ADHD symptoms.

The study appears in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging.

We are now in a phase with enough data to answer some questions about the underlying genetics of a disorder that in the past have been difficult to elucidate, said senior author Damien Fair, Ph.D.

Previous imaging studies had shown different functional connectivity, and we assume those have a genetic basis.

ADHD is a neurodevelopmental psychiatric disorder that affects about 5 percent of children and adolescents and 2.5 percent of adults worldwide. The disorder is characterized by inattentive or hyperactive symptoms with many variations.

The paper focuses on 315 children between the ages of 8 and 12 who participated in a longitudinal ADHD study that began in 2008 at the Oregon Health & Science University in Portland. Fair, a neuroscientist and imaging researcher, and co-author Joel Nigg, Ph.D., a pediatric psychologist participated in the study. Robert Hermosillo, Ph.D., a postdoctoral researcher in Fairs lab, led the study.

The research team selected three areas of the brain based on a brain tissue database that showed where ADHD risk genes were likely to alter brain activity. To measure the brain communication to-and-from these regions on each side of the brain, the researchers used resting-state non-invasive magnetic resonance imaging (MRI) scans.

To begin to bridge genetic and neuroimaging studies of ADHD, researchers used MRI to scan the brains of children. Two regions previously associated with ADHD stood out. In one, a higher ADHD genetic risk correlated with a more active brain circuit anchored by the nucleus accumbens (orange arrow). Interestingly a weaker connection anchored by the caudate nucleus (blue arrow) seemed to protect children at high genetic risk from ADHD behaviors.

Next, they calculated a cumulative ADHD genetic risk score in the children, based on recent genome-wide studies, including a dozen higher-risk genetic regions reported two years ago by a large international collaboration called the Psychiatric Genetics Consortium.

In one brain region anchored by the nucleus accumbens, they found a direct correlation with genetics. Increased genetic risk means stronger communication between the visual areas and the reward centers, explained Hermosillo.

Another brain region anchored by the caudate yielded more puzzling results until the researchers tested its role as a mediator between genetics and behavior.

The less these two regions talk to each other, the higher the genetic risk for ADHD, said Hermosillo. It seems to provide a certain resiliency against the genetic effects of ADHD. Even among those with high risk for ADHD, if these two brain regions are communicating very little, a child is unlikely to end up with that diagnosis.

A third region, the amygdala, showed no correlation between connectivity to the other brain regions and the genetics.

According to the authors, the findings suggest that a genetic score alone will not be enough to predict ADHD risk in individuals because the results show both a genetic and neural contribution toward an ADHD diagnosis.

A future diagnostic tool will likely need to combine genetics and brain functional measures. The brain is not at the mercy of genes, added Hermosillo. Its a dynamic system not preprogrammed for disorders. It has the capacity to change.

Source: Elsevier

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Genetics

RESEARCH THAT MATTERS: Paying attention to the genetic basis for hearing loss key to improving quality of life – TheChronicleHerald.ca

At 12- or 13-years of age, a good student turns bad. He doesnt seem to listen in class. Hes restless.

The boy in this story is a real one. He grew up in an isolated community on the South Coast of Newfoundland, where the genetic lines run deep through many generations.

Dr. Terry-Lynn Young, a member of the gene dream team at Memorial University in St. Johns, first heard about the lad more than 20 years ago.

He started acting out. A hearing test showed he had trouble hearing low frequency sounds. He had a male teacher, and he simply couldnt hear him well.

It turned out the hearing loss was a genetic legacy and the cause of the sudden onset of his troubles at school.

Young was a postdoctoral fellow and member of the Memorial team that worked with members of the boys family, several of whom wore hearing aids.

Anne Griffin, an audiologist on Youngs team confirmed low-frequency hearing loss in family members. Unfortunately, the hearing aids had been tuned to amplify high-pitched sounds.

The audiologist adjusted the aids, cranking up the volume of low frequency sounds. Grown men came out of her office with tears in their eyes. They could finally hear, says Young, a leading geneticist who spent her formative years in St. Anthony, at the top of Newfoundlands Great Northern Peninsula.

The Memorial team conducted genetic testing, finally finding the gene that had impacted the familys hearing for eight generations.

In 2001, Young and others published the results in Human Molecular Genetics, a journal published by Oxford University Press. Almost two decades later, she is incredibly frustrated that the key insight of that peer-review article has not made its way widely into clinical practice.

The insight was that a patients genetics should form the basis of care for hearing loss from each according to his genome, to each according to his needs.

Care for hearing loss, based on genetic testing, is not complicated as it sounds, either. In some cases, audiologists can simply fine tune hearing devices the same way you do your stereo turn down the bass, turn up the treble, and deliver more sound to the right speaker if required.

But the genetic understanding of hearing loss now goes deeper than that, Dr. Young said.

We can tell if the hearing loss is in one ear or both ears, if it gets worse or stays the same over time, if it is high frequency or low frequency loss, if it is likely to impact people when they are older or younger. Its like we know each and every cell.

The underlying health care issue is urgent. Hearing loss is the most common sensory disorder of all in humans, she says, and is now linked to social isolation, dementia in older people, and learning problems in children.

Young describes the cochlea - the snail shaped portion of the inner ear that converts sound vibrations into nerve impulses to the brain as elegant and beautiful. Its a triumph of genetics that the cochlear system is so well-understood. Its a failure of health care delivery that this understanding isnt better reflected in clinical practice.

A good start at improving care delivery would be easier public access to genetic testing, which can be done from a single strand of hair or saliva sample just like on a TV cop show. How do we roll out genetic testing at Costco?, Young asked.

Another step forward would be better training in genetics for student audiologists. Thats sorely lacking today. As a result, audiologists use standard hearing tests, which often fall short of what is needed and as the family from the South Coast of Newfoundland learned the hard way.

As part of Memorials team of geneticists, Young knows that genetic breakthroughs can sometimes result in better patient care in a hurry.

She and her colleagues identified a genetic anomaly in a Newfoundland family that caused sudden cardiac arrest and often early death especially among males. Your first symptom could be your last, she said.

Cardiologists implanted defibrillators in these patients - to restart the heart in case of an incident before Youngs team found the underlying gene.

That was brilliant, she said. The caregivers were out in front of the genetic knowledge, not trailing it.

Young is determined to see genetics play a more significant role in treating hearing care as well.

Im going to beat this drum loud enough that everyone hears she said.

Research That Matters is written by Jim Meek, Public Affairs Atlantic, on behalf of the Association of Atlantic Universities (AAU).

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RESEARCH THAT MATTERS: Paying attention to the genetic basis for hearing loss key to improving quality of life - TheChronicleHerald.ca

Genetics

Yann Joly on the fight against genetic discrimination – McGill Reporter

Yann Joly, Research Director of the Centre of Genomics and Policy

Research Director of the Centre of Genomics and Policy and Associate Professor at the Department of Human Genetics, Yann Joly is a Lawyer Emeritus from the Quebec Bar and a Fellow of the Canadian Academy of Health Sciences. He is currently a member of the Quebec task force on theCOVID-19 Biobank.

Last week, Joly and his collaborators from 16 countries announced the establishment of the international Genetic Discrimination Observatory (GDO). A world first, the GDO is an online platform committed to preventing the misuse of a patients genetic information. This is particularly important within the current context of the COVID-19 pandemic when researchers are collecting samples and data from patients in order to better understand this new disease and develop effective vaccines or therapeutics.

In this Q&A, Joly gives readers more information on genetic discrimination and what is being done to combat it.

Genetic discrimination (GD) means treating people differently from the rest of the population or unfairly profiling them based on actual or presumed genomic and other predictive medical data. The genetic information contained in an individuals DNA can uniquely identify or provide some information about a person, including future probabilities that this individual will develop diseases. Other predictive health information, such as biomarkers, can also be used to discriminate and should also be considered under the GD heading.

This information can be of interest to third parties like insurers, employers, or government officials. Like sexual, ethnic or disability-based discrimination, genetic discrimination is a source of exclusion and can limit the social and professional opportunities of a person thus becoming a source of psychological distress.

There are documented cases of GD reported in studies carried out in a limited number of countries based on predictive test results and family history for a handful of severe single-gene conditions in the context of life insurance or employment. The available evidence is fragmentary, and the methodology used in many studies is inconsistent.

The Genetic Non-Discrimination Act (hereinafter S-201) was passed in April 2017 and is currently applicable in Canada. While it does not solve all the challenges posed by genetic discrimination, it is an important first step. The Act generally makes it a criminal offense to require a person to undergo a genetic test or to report the results as a condition precedent to the provision of goods and services. However, the Quebec Court of Appeal recently declared that the core elements of S-201 were not constitutionally valid.

This decision was appealed to the Supreme Court of Canada and we are currently waiting for their decision on the matter. In the meantime, S-201 continue to be applied. If the Supreme Court is of a similar opinion to that of the Court of Appeal, it could be invalidated.

In addition to the protection provided by S-201, Canadian privacy laws would fully apply to genetic data, which is considered personal information.

Genetic information is increasingly shared across national borders or transcending them, thus limiting the effectiveness of protections built solely around national approaches. Strictly legal solutions, because they tend to be static, are also challenged to keep pace with rapidly evolving science such as genetics.

At its core discrimination is a social phenomenon that needs to be addressed collaboratively and internationally by all stakeholders. The GDO will provide the platform to undertake this important work, which will include documenting instances of genetic discrimination, identifying most effective preventing measures and conveying information, tools and good practices to all stakeholders including the public.

COVID-19 presents Quebecers with an unprecedented health threat that requires us to stand together as a society and take action to protect one another and help find medical solutions to the disease. The COVID-19 Biobank provides us a unique opportunity to learn more about the biological foundations of the disease, individuals at risk and preventive solutions.

The risk of discrimination associated with providing a biological sample and medical information to the Biobank is very small. The data provided is research information that is not clinically validated and should be of no interest to most third parties. Moreover, the collected information is coded, and protected by confidentiality laws and robust security measures. Furthermore, data access will be subject to ethics approval and in some cases controlled access measures.

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Yann Joly on the fight against genetic discrimination - McGill Reporter