Category Archives: Genetics

Genetics

Alnylam Uncovers Genetic Mutations in INHBE That Protect Against Abdominal Obesity – Business Wire

CAMBRIDGE, Mass.--(BUSINESS WIRE)--Alnylam Pharmaceuticals, Inc. (Nasdaq: ALNY), the leading RNAi therapeutics company, announced today that the Company and collaborators have identified mutations in the INHBE gene associated with protection against abdominal obesity and metabolic syndrome a condition impacting more than 20 percent of adults worldwide. The discovery leveraged sequencing data from more than 360,000 individuals in UK Biobank, and was published in the 13th issue of Nature Communications. The published data show that rare mutations in the liver-expressed INHBE gene are associated with lower waist-to-hip ratio adjusted for body mass index (WHRadjBMI), a surrogate for abdominal fat that is causally linked to type 2 diabetes and coronary heart disease. Findings support the potential of INHBE to be evaluated as a novel therapeutic target for the treatment of cardiometabolic disease. The Company plans to pursue a development candidate for INHBE and its gene product, Activin E, leveraging its liver IKARIA platform.

We are thrilled that our investment in genetic databases like UK Biobank is proving to be fruitful in identifying novel targets in highly prevalent diseases with continued unmet need, said Paul Nioi, Ph.D., Vice President, Discovery and Translational Research, and the Leader of Alnylams Human Genetics Group. There is a well-established causal link between increased waist-to-hip ratio and a persons risk of cardiometabolic conditions. By exploring the genetic determinants of waist-to-hip ratio in this study, important insights into the mechanisms that contribute to body fat distribution were uncovered helping identify potential therapeutic targets for abdominal obesity, like INHBE. The results of this exome-wide analysis suggest that targeting INHBE is predicted to have broad beneficial effects on all facets of metabolic syndrome with potential reductions in the risk of type 2 diabetes and coronary heart disease. We are currently testing this hypothesis, with the goal of pursuing a development candidate targeting INHBE in the near future.

We are delighted to see that the uniquely detailed data within UK Biobank - generously donated by our half a million participants - is accelerating research into important health conditions. Thanks to the collaboration with leading life sciences companies in the UK Biobank Exome Sequencing Consortium, the UK Biobank resource is helping to rapidly identify new therapeutic targets for abdominal obesity, said Professor Naomi Allen, UK Biobank Chief Scientist.

Using whole exome-sequencing data from UK Biobank, Alnylam and collaborators mined for gene variants associated with lower WHRadjBMI in more than 360,000 individuals of European ancestry, revealing loss of function in INHBE as a novel genetic factor contributing to a healthier fat distribution. Rare predicted loss of function (pLOF) variants in INHBE, were carried by one in 587 individuals and were associated with lower abdominal fat. In vitro characterization of the most common INHBE pLOF variant in the study, indicated an approximately 90% reduction in secreted activin E levels. Further analysis of INHBE pLOF carriers revealed a favorable metabolic profile, including decreased triglycerides, increased high-density lipoprotein cholesterol, and decreased fasting glucose. There were no associations suggesting adverse effects of INHBE pLOF, and carriers of these variants did not show evidence of excess mortality. The study also detected associations with lower WHRadjBMI for variants in ACVR1C, encoding an activin receptor, further highlighting the involvement of activins in regulating fat distribution.

About UK Biobank

UK Biobank is a large-scale biomedical database and research resource, containing in-depth genetic and health information from half a million UK participants. The database, which is regularly augmented with additional data, is globally accessible to approved researchers and scientists undertaking vital research into the most common and life-threatening diseases. UK Biobanks research resource is a major contributor to the advancement of modern medicine and treatment and has enabled several scientific discoveries that improve human health.

The UK Biobank Exome Sequencing Consortium (UKB-ESC)

In 2018, Alnylam and partners Regeneron, AbbVie, AstraZeneca, Biogen, and Pfizer announced an agreement with UK Biobank to form the UK Biobank Exome Sequencing Consortium (UKB-ESC), a pre-competitive consortium that aims to sequence the whole exomes of 500,000 volunteer participants in the biomedical resource. The goal of the consortium, which represents the largest ever effort to use genome sequencing to map the DNA of a group of people, is to uncover insights that allow researchers to pinpoint new drug targets at the core of human disease in order to develop effective treatments for patients. To date, the UKB-ESC has made whole-exome sequencing data from 450,000 participants available to the global health community for research purposes and will continue to make all sequenced data available at no cost under the terms of the UKB-ESC charter and the founding principles of UK Biobank.

About Cardiometabolic Disease

Cardiometabolic diseases are the number one cause of death in the world; these include but are not limited to cardiovascular disease, obesity, diabetes mellitus, and non-alcoholic fatty liver disease. An estimated 47 million people in the U.S. alone are living with some form of cardiometabolic disease. Despite the availability of many well-established treatments for cardiometabolic diseases, the substantial mortality associated with this group of diseases underscores the high unmet medical need for new therapeutic options, including those directed to novel disease-modifying targets, and with potential to address poor medication adherence.

About IKARIA Platform

Alnylams IKARIA platform takes advantage of more than two decades of experience in developing RNAi therapeutics. IKARIA enables an extended duration of activity in preclinical studies, with potential for annual dosing in humans, and has design features which provide exquisite specificity, further widening the potential therapeutic index, with enhanced target reduction levels.

About RNAi

RNAi (RNA interference) is a natural cellular process of gene silencing that represents one of the most promising and rapidly advancing frontiers in biology and drug development today. Its discovery has been heralded as "a major scientific breakthrough that happens once every decade or so," and was recognized with the award of the 2006 Nobel Prize for Physiology or Medicine. By harnessing the natural biological process of RNAi occurring in our cells, a new class of medicines, known as RNAi therapeutics, is now a reality. Small interfering RNA (siRNA), the molecules that mediate RNAi and comprise Alnylam's RNAi therapeutic platform, function upstream of todays medicines by potently silencing messenger RNA (mRNA) the genetic precursors that encode for disease-causing or disease pathway proteins, thus preventing them from being made. This is a revolutionary approach with the potential to transform the care of patients with genetic and other diseases.

About Alnylam Pharmaceuticals

Alnylam (Nasdaq: ALNY) has led the translation of RNA interference (RNAi) into a whole new class of innovative medicines with the potential to transform the lives of people afflicted with rare and prevalent diseases with unmet need. Based on Nobel Prize-winning science, RNAi therapeutics represent a powerful, clinically validated approach yielding transformative medicines. Since its founding 20 years ago, Alnylam has led the RNAi Revolution and continues to deliver on a bold vision to turn scientific possibility into reality. Alnylams commercial RNAi therapeutic products are ONPATTRO (patisiran), GIVLAARI (givosiran), OXLUMO (lumasiran), AMVUTTRA (vutrisiran), and Leqvio (inclisiran) being developed and commercialized by Alnylams partner, Novartis. Alnylam has a deep pipeline of investigational medicines, including six product candidates that are in late-stage development. Alnylam is executing on its Alnylam P5x25 strategy to deliver transformative medicines in both rare and common diseases benefiting patients around the world through sustainable innovation and exceptional financial performance, resulting in a leading biotech profile. Alnylam is headquartered in Cambridge, MA. For more information about our people, science and pipeline, please visit http://www.alnylam.com and engage with us on Twitter at @Alnylam, on LinkedIn, or on Instagram.

Alnylam Forward Looking Statements

Various statements in this release concerning Alnylam's future expectations, plans and prospects, including, without limitation, Alnylams views with respect to pursuing INHBE as a therapeutic target for cardiometabolic disease and its goal to identify a development candidate targeting INHBE in the near future, Alnylams aspiration to become a leading biotech company, and the planned achievement of its Alnylam P5x25 strategy, constitute forward-looking statements for the purposes of the safe harbor provisions under The Private Securities Litigation Reform Act of 1995. Actual results and future plans may differ materially from those indicated by these forward-looking statements as a result of various important risks, uncertainties and other factors, including, without limitation: the direct or indirect impact of the COVID-19 global pandemic or any future pandemic on Alnylams business, results of operations and financial condition and the effectiveness or timeliness of Alnylams efforts to mitigate the impact of the pandemic; the potential impact of the recent leadership transition on Alnylams ability to attract and retain talent and to successfully execute on its Alnylam P5x25 strategy; Alnylam's ability to discover and develop novel drug candidates, including a development candidate targeting INHBE, and delivery approaches, and successfully demonstrate the efficacy and safety of its product candidates; the pre-clinical and clinical results for its product candidates; actions or advice of regulatory agencies and Alnylams ability to obtain and maintain regulatory approval for its product candidates, as well as favorable pricing and reimbursement; successfully launching, marketing and selling its approved products globally; delays, interruptions or failures in the manufacture and supply of its product candidates or its marketed products; obtaining, maintaining and protecting intellectual property; Alnylams ability to successfully expand the indication for OXLUMO, ONPATTRO and AMVUTTRA in the future; Alnylam's ability to manage its growth and operating expenses through disciplined investment in operations and its ability to achieve a self-sustainable financial profile in the future without the need for future equity financing; Alnylams ability to maintain strategic business collaborations; Alnylam's dependence on third parties for the development and commercialization of certain products, including Novartis, Sanofi, Regeneron and Vir; the outcome of litigation; the potential impact of current and the risk of future government investigations; and unexpected expenditures; as well as those risks more fully discussed in the Risk Factors filed with Alnylam's most recent Quarterly Report on Form 10-Q filed with the Securities and Exchange Commission (SEC) and in its other SEC filings. In addition, any forward-looking statements represent Alnylam's views only as of today and should not be relied upon as representing its views as of any subsequent date. Alnylam explicitly disclaims any obligation, except to the extent required by law, to update any forward-looking statements.

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Alnylam Uncovers Genetic Mutations in INHBE That Protect Against Abdominal Obesity - Business Wire

Genetics

Humans wear cotton every day now, the plant needs genetics’ help to survive – Inverse

Products derived from the cotton plant show up in many items that people use daily, including blue jeans, bedsheets, paper, candles, and peanut butter. In the United States, cotton is a $7 billion annual crop grown in 17 states from Virginia to Southern California. Today, however, its at risk.

Cotton plants from fields in India, China, and the U.S. the worlds top three producers grow, flower, and produce cotton fiber very similarly. Thats because they are genetically very similar.

This can be a good thing since breeders select the best-performing plants and cross-breed them to produce better cotton every generation. If one variety produces the best-quality fiber that sells for the best price, growers will plant that type exclusively. But after many years of this cycle, cultivated cotton all starts to look the same: high-yielding and easy for farmers to harvest using machines, but wildly underprepared to fight disease, drought, or insect-borne pathogens.

Breeding alone may not be enough to combat the low genetic diversity of the cultivated cotton genome, since breeding works with what exists, and what exists all looks the same. And genetic modification may not be a realistic option for creating cotton that is useful for farmers, because getting engineered crops approved is expensive and heavily regulated. My research focuses on possible solutions at the intersection of these tools.

In a perfect world, scientists could change just a few key components of the cotton genome to make plants more resilient to stresses such as pests, bacteria, fungi, and water limitations. And the plants would still produce high-quality cotton fiber.

Heres the background This strategy isnt new. Some 88 percent of the cotton grown in the U.S. has been genetically modified to resist caterpillar pests, which are expensive and hard to manage with traditional insecticides. But as new problems emerge, new solutions will be required that will demand more complex changes to the genome.

Recent advances in plant tissue culture and regeneration make it possible to develop a whole new plant from a few cells. Scientists can use good genes from other organisms to replace the defective ones in cotton, yielding cotton plants with all the resistance genes and all the agriculturally valuable genes.

The problem is that getting regulatory approval for a genetically modified crop to go to market is a long process, often 8 to 10 years. And its usually expensive.

Genetic modification isnt the only option. Researchers today have access to a gigantic amount of data about all living things. Scientists have sequenced the entire genomes of numerous organisms and have annotated many of these genomes to show where the genes and regulatory sequences are within them. Various sequence comparison tools allow scientists to line up one gene or genome against another and quickly determine where all the differences are.

Plants have very large genomes with lots of repetitive sequences, which makes them very challenging to unpack. However, a team of researchers changed the game for cotton genetics in 2020 by releasing five updated and annotated genomes two from cultivated species and three from wild species.

Having the wild genomes assembled makes it possible to start using their valuable genes to improve cultivated varieties of cotton by breeding them together and looking for those genes in the offspring. This approach combines traditional plant breeding with detailed insights into cottons genome.

We now know which genes we need to make cultivated cotton more resistant to disease and drought. And we also know where to avoid making changes to important agricultural genes.

Blue jeans never go out of style.Jena Ardell/Moment/Getty Images

These genomes also make it possible to develop new screening tools to characterize interspecific hybrids the offspring of two cotton plants from different species. Before this information was available, there were two primary forms of hybrid characterization. Both were based on single nucleotide polymorphisms, or SNPs differences between species in a single base pair, the individual building blocks that make up DNA. Even plants with small genomes have millions of base pairs.

SNPs work well if you know exactly where they are located in the genome, if there are no mutations that change the SNPs, and if there are plenty of them. While cotton has SNPs that have been identified and verified in specific regions of the genome, they are few and far between. So characterizing cotton hybrids by focusing exclusively on SNPs would result in incomplete information about those hybrids genetic composition.

These new genomes open the door for developing sequencing-based screening of hybrids, which is something Ive incorporated into my work. In this approach, scientists still use SNPs as a starting point, but they can also sequence the surrounding DNA. This helps to fill in gaps and sometimes discover new, previously undocumented SNPs.

Sequence-based screening helps scientists make more informed and robust maps of the genomes of hybrids. Determining which parts of the genome are from which parent can give breeders a better idea of which plants to cross together to subsequently create better, more productive cotton in every generation.

As the worlds population rises toward a projected 9.8 billion by 2050, demand for all agricultural products will also rise. But making cotton plants more productive is not the only goal of genetic improvement.

Climate change is raising average global temperatures, and some important cotton-producing regions like the U.S. Southwest are becoming drier. Cotton is already a crop accustomed to heat our research plots can thrive in temperatures as high as 102 degrees Fahrenheit (39 C) but one cotton plant requires about 10 gallons (38 liters) of water over the course of a four-month growing season to achieve its maximum yield potential.

Researchers have started to search for cultivated cotton that can tolerate drought at the seedling stage, and also in hybrid lines and genetically modified lines. Scientists are optimistic that they can develop plants that have higher drought resilience. Along with many other cotton breeders around the world, my goal is to create more sustainable and genetically diverse cotton so that this essential crop can thrive in a changing world.

This article was originally published on The Conversation by Serina Taluja at Texas A&M University. Read the original article here.

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Humans wear cotton every day now, the plant needs genetics' help to survive - Inverse

Genetics

Views of Canadian healthcare professionals on the future uses of non-invasive prenatal testing: a mixed method study | European Journal of Human…

Views of Canadian healthcare professionals on the future uses of non-invasive prenatal testing: a mixed method study | European Journal of Human Genetics  Nature.com

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Genetics

Researchers find new genetic mutation causing autism through study of patients and families – KBR

A Seoul National University Bundang Hospital (SNUBH) research team has discovered a new gene mutation related to the cause of autism for the first time worldwide through a large-scale genetics study of autistic patients and their families.

Autism is a developmental disorder characterized by repetitive behavior or narrowness of interest along with a lack of communication or social interaction, as shown in the popular drama "Extraordinary Attorney Woo." Typically, characteristic symptoms are revealed around the age of 2. Considering the brain develops quickly, early intervention is important.

Genes play a major role in the development of autism, but the specific genes and their role in early brain development have not been identified. Consequently, there are no treatments for autism symptoms, such as social deficits or communication disorders, but only medication to cure impulsivity or anxiety symptoms.

Professor Yoo Hee-jeong of the Neuropsychiatry Department at SNUBH conducted the joint study with Professors Lee Jeong-ho and Choi Jun-kyun of the Korea Advanced Institute of Science and Technology (KAIST), Institute of Basic Science Director Kim Eun-joon, and others to identify the genetic mutations that cause autism for the development of therapeutics.

The joint group focused on the brains non-coding region, a genomic region that accounts for more than 98 percent of the genomic data but was excluded from the study as it does not directly produce proteins. Researchers received blood from 813 people autism patients and their family members suitable for the study and analyzed the genome, produced human stem cells to reproduce prenatal neurons.

Results revealed that genetic mutations in the non-coding region affect brain development by remotely influencing distant genetic mutations through interactions in three-dimensional spaces in early stages of neurodevelopment.

This study changes the autistic research paradigm, which previously focused only on areas encoding existing proteins, and reveals new target genes to determine the root cause of autism. Professor Yoo said.

Yoo added that the team has identified the hidden secret of autism using data unique to Koreans' autism parties and families and are very grateful for the dedication of the participants in this study.

We will continue research to help improve the lives of autistic people and their families, Yoo said.

The study was published in the latest issue of the Molecular Psychiatry journal.

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Researchers find new genetic mutation causing autism through study of patients and families - KBR

Genetics

NIH grant awarded to Marshall researcher for studying genetic mechanisms of cocaine addiction – News-Medical.Net

Price E. Dickson, Ph.D., an assistant professor of biomedical sciences at the Marshall University Joan C. Edwards School of Medicine, has received a $407,000 grant from the National Institutes of Health to study the genetic and genomic mechanisms driving the relationship between social reward and cocaine addiction.

During the two-year R21 grant, Dickson and his research team will study the genetic and genomic mechanisms driving social reward and the preference for a social reward over a drug reward. Social rewards refer to the reinforcing social stimuli that individuals experience during interactions with others. A strong drive to seek out social interactions rather than drugs of abuse may confer addiction resistance, whereas the absence of this drive may result in addiction vulnerability, Dickson explains.

"Despite the importance of social rewards in addiction, the genetic mechanisms underlying variation in the preference for a social reward over a drug reward have been unexplored," Dickson said. "Because the mouse genome is very similar to the human genome, genetic studies using mice can provide valuable information about the genetics underlying human addiction."

To model the vast genetic diversity in humans, the team will use mice from the Collaborative Cross mouse panel, which contains almost all of the genetic diversity present in both wild and laboratory mice. To identify the genetic mechanisms underlying the preference for social interactions rather than addictive drugs, individual Collaborative Cross mice will have the choice to intravenously self-administer cocaine or to briefly interact with another mouse. Single-cell RNA sequencing will then be used to identify genetic signatures associated with these preferences in the reward circuitry of the brain.

"The successful completion of this project will provide a foundation for future deep characterization of identified genetic mechanisms driving the preference for a social reward over a drug reward in mice and contribute to the development of novel, more effective addiction treatments, Dickson said."

Since joining Marshall's faculty in 2020, Dickson has authored or co-authored four publications in academic journals and four presentations at scientific conferences. He is a recipient of a 2020 K99/R00 program grant from the National Institute on Drug Abuse to further his research on the genetic relationship between stress and addiction. Dickson joined the School of Medicine faculty in June 2020, following seven years of postdoctoral research at the Jackson Laboratory in Bar Harbor, Maine.

The grant (1R21DA054929-01A1) was announced July 12 by U.S. Senators Joe Manchin (D-WV) and Shelley Moore Capito (R-WV).

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NIH grant awarded to Marshall researcher for studying genetic mechanisms of cocaine addiction - News-Medical.Net

Genetics

Explained| Genetics and its Mendelian inheritance – The Hindu

Long before genes, genomes and genetics were known, Augustinian monk Gregor Mendel established three principles of inheritance from his experiments on pea plants.

Long before genes, genomes and genetics were known, Augustinian monk Gregor Mendel established three principles of inheritance from his experiments on pea plants.

Its a commonly observed habit in families to draw likenesses between members of the youngest generation and their ancestors. This baby has a smile like her mother, one would say, or, He has exactly the temperament of his grandfather. This project may be extended by some to even saying, X writes so well, she has inherited this from her eldest aunt. If someone should be outstandingly brilliant in math or history, quick follows the comment Its all in the genes.

Now, many of these traits may not be heritable, or little is known about whether they are inherited. So these statements often are mere speculations; however, they are speculations supported by a pervasive and instinctive knowledge of the laws of genetics and the mechanism of genes and heredity. Of course, its one thing to pull out statements like this based on purely anecdotal occurrences and quite another to demonstrate them through years of careful experimentation.

The latter is what Gregor Mendel did. In the 1860s, much before the gene was discovered or the term genetics was coined, Mendel, a monk of the order of St. Augustine, discovered the cornerstone of genetics the laws of Mendelian inheritance using a methodical approach that is the envy of scientists even today. For this, he later came to be celebrated as the father of genetics.

For eight years, starting with 22 pea plants, he and his disciples allowed the plants to self-pollinate and cross-pollinate and came up with around 10,000 descendent plants. By observing them, Mendel came up with three laws. The first of these is the principle of uniformity all the progeny of a cross between plants that differ in only one trait will look alike. This can be understood as follows if the parent plants differ by only one trait say, one has wrinkled seeds and one has round seeds but are alike in all other aspects, the progeny will all have round seeds or all have wrinkled seeds depending on which trait is dominant. It was Gregor Mendel who first introduced the concepts of dominant and recessive traits.

But he believed, and showed experimentally, that the progeny contain the other traits within them and pass them on to subsequent generations. Continuing our previous example, if the four identical-looking plants from generation two, all with round seeds, were cross-fertilized, their offspring would have a mix of round and wrinkled seeds in a 3:1 ratio. This showed that even though they themselves had only round seeds, they carried in them something, let us say particles, that passed on the trait to their offspring.

Based on the above concept, Mendel put forth the second principle of inheritance, which is that the particles which determine these traits are separated during meiosis into gametes, and that meiosis produces an equal number of egg or sperm cells that contain particles carrying each trait.

The third principle he laid down was the principle of independent assortment, which statesthat alleles of one locus segregate into gametes independently of alleles of other loci. This means the choiceof one trait (say round or wrinkled seeds) does not affect the passing on of choices of a different trait (such as white or purple flowers).

With these laws, Mendel established the foundation of genetics even though he did not know anything about genes, genomes and genetics. No wonder, then, that he is known as the father of genetics. He submitted these findings and his observations of eight years in 1865 to the relatively lesser-known journal published by the Natural History Society of Brno (now in the Czech Republic).The paper was not noticed or celebrated much when he was alive. When Mendel died in 1884, all his papers were burnt, making it really difficult to trace out his contributions.

Decades later, in 1900, Mendels paper was independently discovered by three scientists working in the field. Further work has revealed much more complex details of genetics and inheritance, but Mendel has a place that cannot be denied.

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Explained| Genetics and its Mendelian inheritance - The Hindu

Genetics

Is alcoholism genetic? Everything you need to know as Vicky Pattinson opens up about her battles – Evening Standard

V

icky Pattison has opened up about her struggle with alcohol and said she was scared to have kids who felt broken like her.

The former Geordie Shore star, 34, has been working with Channel 4 on a documentary about her father, who is an alcoholic and her own relationship with alcohol.

During an interview with Skys Beth Rigby, Vicky admitted to having an addictive personality, adding that she was scared of history repeating itself, as her father is an alcoholic.

Vicky explained that she was unable to live a balanced life and was often self-sabotaging. The media personality said: I always worried because Im like him in a lot of ways and I was aware that I had an addictive personality.

Speaking about her fears around having children, Vicky said: I was also just really scared that I was going to have children who felt in some way broken like me.

But the documentary has brought us a lot of peace and clarity.

But, what is alcoholism, and is it genetic? Heres everything you need to know.

What is alcoholism?

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines alcohol dependency as a form of problem drinking that has become severe, with compulsive behaviors and physical dependence associated with the condition.

What causes alcoholism?

Typically, alcohol addiction is considered to involve several complex risk factors:

Stress in ones work or home life may trigger an addiction. When the person drinks alcohol, for example, they may feel relaxed and happy compared to the stress they feel when they are sober. This reinforces the desire to use alcohol as a coping mechanism for stress.

Those who have mental illnesses, especially anxiety, depression, bipolar disorder, and schizophrenia are very likely to struggle with co-occurring alcohol use disorder.

Women are at risk of developing alcoholism faster than men due to differences in body mass, hormones, and metabolism.

Is alcohol dependecy genetic?

Genetics and family history are the most correlated with risk of alcohol dependency, in fact, genetic risk is about half of the problem, while family history is the other half.

Certainly, genetics are passed down through families, but family history also includes the environment in which one was raised. Childhood abuse, parental struggles, and mental illness in close family members all contribute to the risk of developing an addiction to drugs or alcohol.

These are numerous genes found to be associated with substance abuse, including alcoholism. Some genes can help a person regulate their alcohol consumption or avoid the substance altogether; others increase the persons risk of abusing alcohol.

Gene expression is also affected by environment. If a person grows up in a house with a parent who abuses drugs, struggles with mental illness, suffers a major financial setback or similar stress, and the child has a gene linked to alcohol use disorder, they are very likely to develop this condition later in life.

Prevention and education programs can address this risk as part of regular medical checkups. Genetics are understood to be a component of AUD, but not the sole cause.

If youre struggling with alcohol abuse, there are some useful tips on the NHS website for support.

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Is alcoholism genetic? Everything you need to know as Vicky Pattinson opens up about her battles - Evening Standard

Genetics

Population genomics of Group B Streptococcus reveals the genetics of neonatal disease onset and meningeal invasion – Nature.com

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Genetics

Cruchaga named Morriss Professor Washington University School of Medicine in St. Louis – Washington University School of Medicine in St. Louis

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Studies genetic architecture of neurodegenerative diseases

Carlos Cruchaga, PhD, has been named the Barbara Burton and Reuben M. Morriss III Professor at Washington University School of Medicine in St. Louis. Shown at his installation ceremony are (from left) David H. Perlmutter, MD, executive vice chancellor for medical affairs and dean of the School of Medicine; Cruchaga; and Chancellor Andrew D. Martin.

Carlos Cruchaga, PhD, a pioneer in the use of human genomic data to understand and elucidate the biology of neurodegenerative diseases such as Alzheimers disease, has been named an inaugural Barbara Burton and Reuben M. Morriss III Professor at Washington University School of Medicine in St. Louis.

Cruchaga was installed by Chancellor Andrew D. Martin and David H. Perlmutter, MD, executive vice chancellor for medical affairs, the George and Carol Bauer Dean of the School of Medicine and the Spencer T. and Ann W. Olin Distinguished Professor.

The professorship was created through a bequest from the late Reuben M. Morriss III and Barbara Burton Morriss to Washington University, to advance Alzheimers disease research.

The Morrisses were devoted members of the St. Louis community, and their investment in Washington University and specifically in Alzheimers research has created three endowed professorships bearing their names, Martin said. Through their generous gift to the university, they will continue to have a powerful impact on research and teaching at the university in perpetuity.

Added Perlmutter: We are deeply grateful to Barbara and Reuben Morriss for investing in Washington University and in our work to advance the understanding and treatment of Alzheimers disease. We look forward to future discoveries from the Cruchaga lab as Carlos combines complex technologies to identify genetic variants that may contribute to Alzheimers, Parkinsons disease and other devastating disorders.

Cruchagas research focuses on leveraging data from genetics, genomics and other omics and integrating that information with findings from neuroimaging and neuropathology to identify novel genes, biological pathways, molecular biomarkers and drug targets that may generate new approaches to diagnosing and treating neurodegenerative illnesses.

Carlos came to Washington University as a postdoc to study the genetics of neurodegenerative illnesses, said Charles F. Zorumski, MD, the Samuel Guze Professor and head of the Department of Psychiatry. In 2014, Carlos became the leader of the genetics group at the Knight Alzheimer Disease Research Center (ADRC) and at the Hope Center for Neurological Disorders in the Department of Neurology. And last year he became the founding director of the Neurogenomics and Informatics Center, pioneering approaches to improve the understanding of causes and potential treatments for these devastating illnesses.

Cruchaga has published more than 270 manuscripts and is the principal investigator on six grants funded by the National Institutes of Health (NIH). He is a core leader for the biobank and genetics core of the international Dystonia Coalition; the Aging Adult Brain Connectome project; the Alzheimers Biomarkers Consortium-Down Syndrome; the Knight ADRC genetics core; and the Dominantly Inherited Alzheimer Network (DIAN) genetics core.

Cruchaga earned his doctorate in biochemistry and molecular biology in 2005 at the University of Navarra in Pamplona, Spain. As a postdoc, he trained in quantitative human genomics in the laboratory of Alison Goate, DPhil, at Washington University. He established his own laboratory in 2011. His key aim has been to leverage genetics, multi-omics and functional genomics studies in neurodegeneration and diseases of the central nervous system and to translate those into improvements in human health by better understanding the molecular underpinnings of disease.

It is quite an honor to have our work recognized in this way, Cruchaga said. We have been attempting to leverage a great deal of information to identify treatments that might make a big difference in the lives of millions of people affected by Alzheimers disease and other neurodegenerative disorders. This endowment allows us to advance that work, help patients and provide hope for those affected by some very distressing diseases.

A graduate of Saint Louis Country Day School in Ladue, Mo., and Princeton University in New Jersey, Reuben Morriss III earned a law degree from Washington University in 1964. He joined Boatmens Bank, beginning a long career as a leader of the St. Louis financial sector. He eventually became chairman and president of Boatmens Trust Co., a position he held until his retirement in 1995. He was a board chair of Mary Institute and Saint Louis Country Day School and of William Woods University in Fulton, Mo. He also served on the boards of St. Lukes Hospital in Chesterfield, Mo., and the St. Louis Bi-State American Red Cross.

Barbara Burton Morris was a graduate of John Burroughs School in Ladue, and Briarcliff College in Westchester County, N.Y. She was a board member of the Alzheimers Association and the Central Institute for the Deaf, and she donated time and resources to many other local charitable and cultural institutions.

The couple was married for 48 years and had two children, Burton Douglass Morriss and Barbara Dulany Morriss; and five grandchildren. Reuben Morriss III died in 2006, and Barbara Burton Morriss died in 2018.

Washington University School of Medicines 1,700 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, and currently is No. 4 in research funding from the National Institutes of Health (NIH). Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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Cruchaga named Morriss Professor Washington University School of Medicine in St. Louis - Washington University School of Medicine in St. Louis

Genetics

Lifestyle or Genetics: Which is More Important for Heart Health? – One Green Planet

It has been a busy day in the Emergency Department. Doctors, nurses, and other staff are bustling about, doing their best to provide excellent care for every patient. Dialogue fills the nursing stations with background noise. I am walking from room to room, tending to several patients, performing my initial evaluation on some, and providing test results to others. As I finally take a few moments to sit down in front of my computer and do some charting, the nurse in charge hands me the EMS phone.

The paramedic at the other end of the line informs me that they are en route with a 54-year-old male having severe chest pain and difficulty breathing. They have obtained an EKG that is concerning and have given him medications to treat his pain. Their estimated arrival time at our hospital will be in approximately ten minutes.

Upon receiving this report, I spring into action. I notify the nurses, and we begin preparing a room to care for our next patient, setting up monitors, IV start kits, and other resuscitative equipment. The ambulance pulls into the garage, and within another moment, the doors slowly swing open, and the crew rolls in. A dark-haired man is sitting up and leaning forward on the stretcher. Beads of sweat roll down his forehead, and he appears moderately distressed as he clutches his chest.

I greet my patient, Hi, Im Dr. Piriano. When did your symptoms begin?

He looks at me with fear in his eyes. Im so scared.

I know. I place my hand on his shoulder. Dont worry. Were going to help you.

I started to feel pressure in my chest about an hour ago. I feel nauseous, and Im having trouble breathing.

OK, got it. Were going to be doing a lot of things really quickly to take care of you. As I utter these words, a technician has already connected the patient to an EKG machine and is printing out the electrical tracing of his heartbeats. Once complete, she tears the paper from the machine and hands it to me. The pattern on the pink sheet is unmistakablethis man is indeed having a heart attack.

I explain the EKG findings to my patient and tell him that he will need a cardiac catheterization to find the blocked artery and place a stent to open it and restore blood flow to his heart. He is given heart-protective medications, the cardiologist is called, and he is soon whisked off to the catheterization suiteall within thirty minutes from the time he entered the Emergency Department. It is rewarding to know that this gentleman will receive a new lease on life. Modern medicine is undoubtedly incredible, and I am in awe knowing how much progress humans have made. It is truly miraculous to witness the coordinated efforts of a team of people acting so swiftly to save another persons life.

However, I still have one critical questiondid this persons heart attack have to happen at all? The answer to this question is where the story changes from one of suffering to one of hope.

My fictional patient, like millions of real people, has heart disease. Coronary artery disease (CAD) is the most common type of heart disease. It is caused by plaque build-up in the arteries supplying the heart with life-giving oxygen and nutrients, causing these blood vessels to narrow. The most recent statistic from February of 2022 reveals that about 18.2 million adults in the United States age 20 and older have CAD. Although this is certainly a harrowing fact, it can be drastically changed.

How so?

To answer this question, we have to look at the causes of CAD. Without getting into the details of the mechanisms of plaque build-up, suffice it to say that the major players in the development of CAD are cholesterol and inflammation. Thus, if we can lower these two things, we can also reduce our chances of plaque formation. Sounds greatbut how can we do this? The answer is that it all comes down to lifestyle, as levels of cholesterol and inflammation are intimately connected to how we live and what we eat.

Some people may object, citing bad genetics and stating that they have a strong family history of heart disease. They may note multiple relatives who suffered heart attacks at fairly young ages. It doesnt matter what I do. Im doomed to have a heart attack, they may state. On the surface, it may seem as though they have a valid point. However, digging deeper will reveal an entire realm of evidence and knowledge that refutes this belief.

Does lifestyle play a more important role in the health of our hearts than our genes do? Lets take a brief look at some of the research. One of the most prominent figures in this area of study is Dr. Dean Ornish. For more than three decades, Dr. Ornish and his colleagues, in collaboration with major academic institutions, have been conducting research studies investigating the effects of lifestyle on well-being. The participants in their studies made lifestyle changes that consisted of a low-fat vegetarian diet, aerobic exercise, stress management, smoking cessation, and group psychosocial support. Their results were nothing short of remarkable. Thus far, I have been speaking about the prevention of heart disease. These studies demonstrated that a healthy lifestyle could reverse heart disease that has already developed. Amazing! Two of these research papers have been published in the Journal of the American Medical Association and The Lancet. Another study also showed that lifestyle changes, such as those mentioned, improved many of the risk factors that lead to heart disease, such as body weight, blood pressure, and cholesterol.

Even more exciting is the fact that such lifestyle changes not only reduce the risk factors for heart disease but also affect our DNA. A field of science called epigenetics explores how our environments affect our genes. Moreover, it appears that genes have switches and can be activated and inactivated by environmental cues, such as our lifestyles. In other words, live an unhealthy lifestyle, and disease-preventing genes may be deactivated while disease-promoting genes may be activated. Conversely, live a healthy lifestyle, and the opposite may occur. One study examining prostate cancer found that lifestyle changes affected the expression of over 500 genes.

This information is truly powerful and inspiring. It provides evidence that we are not victims of our genes. An individual is not doomed to have a heart attack solely because many family members have already suffered through one. By changing our lifestyles, we can prevent disaster. We can control our destinies and our lives. We have that capability, and there is extraordinary hope in that.

Reducing your meat intake and eating more plant-based foods is known to help withchronic inflammation,heart health,mental wellbeing,fitness goals,nutritional needs,allergies,gut health,andmore! Unfortunately, dairy consumption also has been linked to many health problems, includingacne,hormonal imbalance,cancer, and prostate cancer,and has manyside effects.

For those interested in eating more plant-based, we highly recommend purchasing one of our manyplant-based cookbooksor downloading theFood Monster Appwhich has thousands of delicious recipes making it the largest vegan recipe resource to help reduce your environmental footprint, save animals and get healthy! And, while you are at it, we encourage you to also learn about theenvironmentalandhealth benefitsof aplant-based diet.

Here are some resources to get you started:

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Lifestyle or Genetics: Which is More Important for Heart Health? - One Green Planet