Archive for the ‘Gene Therapy Research’ Category

Public release date: 16-Jul-2012 [ | E-mail | Share ]

Contact: Nathan Hurst hurstn@missouri.edu 573-882-6217 University of Missouri-Columbia

COLUMBIA, Mo. A team of University of Missouri researchers has found that introducing a missing gene into the central nervous system could help extend the lives of patients with Spinal Muscular Atrophy (SMA) the leading genetic cause of infantile death in the world.

SMA is a rare genetic disease that is inherited by one in 6,000 children who often die young because there is no cure. Children who inherit SMA are missing a gene that produces a protein which directs nerves in the spine to give commands to muscles.

The MU team, led by Christian Lorson, professor in the Department of Veterinary Pathobiology and the Department of Molecular Microbiology and Immunology, introduced the missing gene into mice born with SMA through two different methods: intravenously and directly into the mice's central nervous systems. While both methods were effective in extending the lives of the mice, Lorson found that introducing the missing gene directly into the central nervous system extended the lives of the mice longer.

"Typically, mice born with SMA only live five or six days, but by introducing the missing SMN gene into the mice's central nervous systems, we were able to extend their lives 10-25 days longer than SMA mice who go untreated," said Lorson, who works in the MU Bond Life Sciences Center and the College of Veterinary Medicine. "While this system is still not perfect, what our study did show is that the direct administration of the missing gene into the central nervous system provides some degree of rescue and a profound extension of survival."

There are several different types of SMA that appear in humans, depending on the age that symptoms begin to appear. Lorson believes that introducing the missing gene through the central nervous system is a way to potentially treat humans regardless of what SMA type they have.

"This is a treatment method that is very close to being a reality for human patients," Lorson said. "Clinical trials of SMA treatment using gene therapy are likely to begin in next 12-18 months, barring any unforeseen problems."

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The study, "Direct central nervous system delivery provides enhanced protection following vector mediated gene replacement in a severe model of Spinal Muscular Atrophy", was published in Biochemical and Biophysical Research Communications. Co-authors of the study include Jacqueline Glascock and Monir Shababi from MU College of Veterinary Medicine.

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Gene therapy treatment extends lives of mice with fatal disease, MU study finds

By LINDSAY PETERSON | The Tampa Tribune Published: July 16, 2012 Updated: July 16, 2012 - 6:00 AM

Stephen Liggett isn't crazy about the term personalized medicine, though he's been practicing it for nearly two decades as a doctor and scientist.

Good doctors have personalized their treatment for centuries, he said.

But this is different. Game-change different.

The University of South Florida has created a Personalized Medicine Institute and hired Liggett from the University of Maryland to put it together and elevate it to national prominence.

He's in charge of ushering in a fundamentally new kind of health care to Florida. It's based on this idea:

Key information about a person's health and response to drug treatment is locked inside his genetic code, and that information should guide every doctor's treatment decisions.

It's the antithesis to the "one-size-fits-all" approach that dominates health care treatment across the country, Liggett said.

For instance, if you have heart trouble, your doctor will probably prescribe Coumadin, a drug that prevents blood from clotting and precipitating a heart attack or stroke. Millions of people take it.

But if you have a certain genetic makeup, Coumadin could cause fatal side effects.

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USF institute might reform patient diagnosis

Public release date: 15-Jul-2012 [ | E-mail | Share ]

Contact: NINDS press team nindspressteam@ninds.nih.gov 301-496-5751 NIH/National Institute of Neurological Disorders and Stroke

Researchers have linked newly discovered gene mutations to some cases of the progressive fatal neurological disease amyotrophic lateral sclerosis ALS, also known as Lou Gehrig's disease. Shedding light on how ALS destroys the cells and leads to paralysis, the researchers found that mutations in this gene affect the structure and growth of nerve cells.

ALS attacks motor neurons, the nerve cells responsible for controlling muscles. People with ALS experience such early symptoms as limb weakness or swallowing difficulties. In most people, the disease leads to death three to five years after symptoms develop, usually as a result of respiratory failure.

Scientists at the University of Massachusetts Medical School, Worcester, collaborated with international ALS researchers to search for gene mutations in two large families with an inherited form of ALS. The researchers used a technique to decode only the protein-encoding portions of DNA, known as the exome, allowing an efficient yet thorough search of the DNA regions most likely to contain disease-causing mutations. This deep sequencing of the exome led to the identification of several different mutations in the gene for profilin (PFN1) which were present only in the family members that developed ALS. Further investigations of 272 other familial ALS cases across the world showed that profilin mutations were also found in a small subset (about 1 to 2 percent) of the familial ALS cases studied.

The protein profilin is a key part of the creation and remodeling of a nerve cell's scaffolding or cytoskeleton. In fly models, disrupting profilin stunts the growth of axons the long cell projections used to relay signals from one neuron to the next or from motor neurons to muscle cells. After identifying the PFN1 mutations in ALS patients, the researchers demonstrated that these mutations inhibited axon growth in laboratory-grown motor neurons as well. They also found that mutant profilin accumulated in clumps in neural cells, as has been seen for other abnormal proteins associated with ALS, Parkinson's and Alzheimer's. Neural cells with PFN1 mutations also contained clumps of a protein known as TDP-43. Clumps of abnormal TDP-43 are found in most cases of ALS, further linking profilin to known ALS mechanisms.

John Landers, Ph.D., associate professor of neurology at the University of Massachusetts Medical School, described how studying ALS in large families is challenging. "ALS is a late-onset, rapidly progressive disease. Unless you've been following a family for decades, it is hard to get DNA samples to study," Dr. Landers said. "We were very fortunate to obtain the DNA samples with the help of our research collaborators and the affected families."

Over a dozen genes have been linked to ALS, and these findings support existing studies which suggest that cell cytoskeleton disruptions play a major role in ALS and other motor neuron diseases. Motor neurons are large cells with long axons that connect to muscle, and cytoskeleton proteins are especially important in the transport of proteins along the axon to the remote parts of the neuron. This information could be useful in developing strategies for detection and treatment of ALS.

"In all of the causative genes that we identify, we look for common pathways," Dr. Landers said. "Every time we are able to identify a new gene, we have another piece of the puzzle. Each one of these genes helps us to understand what's going on. The more of these we can find, the more we're going to know about what's going wrong in ALS."

Familial ALS accounts for 10 percent of all ALS cases, but the majority of ALS cases are sporadic, where the cause is unknown. Even though this new mutation is linked to familial ALS, it reveals information about the mechanisms underlying motor neuron degeneration in general, and also may have broader implications for understanding sporadic ALS.

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New gene mutations linked to ALS and nerve cell growth dysfunction

ScienceDaily (July 15, 2012) A new genetic mutation that causes familial amyotrophic lateral sclerosis (ALS), a fatal neurological disorder also known as Lou Gehrig's Disease, has been identified by a team of scientists led by researchers at the University of Massachusetts Medical School (UMMS). Mutations to the profilin (PFN1) gene, which is essential to the growth and development of nerve cell axons, is estimated to account for one to two percent of inherited ALS cases. The finding, described July 15 in the online edition of Nature, points to defects in a neuron's cytoskeleton structure as a potential common feature among diverse ALS genes.

"This discovery identifies what may possibly be a common biological mechanism involved across familial ALS cases regardless of genetics," said John Landers, PhD, associate professor of neurology and senior author of the study. "We know of at least three other ALS genes, in addition to PFN1, that adversely impact axon growth. If indeed, this is part of the disease's mechanism, then it might also be a potential target for therapeutics."

Robert Brown, MD, DPhil, a co-author on the study and chair of neurology at UMass Medical School, said "Dr. Landers has done great work in defining this new pathway for motor neuron death. We are delighted to have identified the defects in families from the U.S., Israel and France that we have been investigating for several years. Our finding is particularly exciting because it may provide new insights into ALS treatment targets."

ALS is a progressive, neurodegenerative disorder affecting the motor neurons in the central nervous system. As motor neurons die, the brain's ability to send signals to the body's muscles is compromised. This leads to loss of voluntary muscle movement, paralysis and eventually respiratory failure. The cause of most cases of ALS is not known. Approximately 10 percent of cases are inherited. Though investigators at UMass Medical School and elsewhere have identified several genes shown to cause inherited or familial ALS, almost 50 percent of these cases have an unknown genetic cause.

The current Nature study details the discovery of the PFN1 gene mutation among two large ALS families. Both families were negative for known ALS-causing mutations and displayed familial relationships that suggested a dominant inheritance mode for the disease. For each family, two affected members with maximum genetic distance were selected for deep DNA sequencing. To identify an ALS-causing mutation, genetic variations between the family members were identified and screened against known databases of human genetic variation, such as the 1000 Genomes Project. This narrowed down the resulting number of candidate, ALS-causing mutations to two within the first family and three within the second. Interestingly, both families contained different mutations within the same gene -- PFN1, the likely causative mutation. With additional screening, the team documented that in a total of 274 families sequenced, seven contained a mutation to the PFN1 gene, establishing it as a likely cause for ALS.

While it is not certain how the PFN1 mutation causes ALS, the cellular functions it controls within the motor neurons are responsible for regulation of a number of activities, including the growth and development of the axon, the slender projection through which neurons transmit electrical impulses to neighboring cells, such as muscle. When introduced into motor neuron cells, normal PFN1 protein was found diffused throughout the cytoplasm. Conversely, the mutant PFN1 observed in ALS patients was found to collect in dense aggregates, keeping it from functioning properly. Motor neurons producing mutated PFN1 showed markedly shorter axon outgrowth.

"The discovery that mutant PFN1 interferes with axon outgrowth was very exciting to us," said Claudia Fallini, PhD, a postdoctoral researcher at Emory University School of Medicine who collaborated with the UMass Medical School authors to investigate PFN1's functions in cultured motor neurons. "It suggests that alterations in actin dynamics may be an important mechanism at the basis of motor neuron degeneration."

"In healthy neurons, PFN1 acts almost like a railroad tie for fibrous filaments called actin, which make up the axon" said Landers. "PFN1 helps bind these filaments to each other, promoting outgrowth of the axon. Without properly functioning PFN1 these filaments can't come together. Here we show that mutant PFN1 may contribute to ALS pathogeneses by accumulating in these aggregates and altering the actin dynamics in a way that inhibits axon outgrowth."

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Disruption of cytoskeleton pathways contribute to amyotrophic lateral sclerosis pathogenesis

Public release date: 15-Jul-2012 [ | E-mail | Share ]

Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School

WORCESTER, Mass. A new genetic mutation that causes familial amyotrophic lateral sclerosis (ALS), a fatal neurological disorder also known as Lou Gehrig's Disease, has been identified by a team of scientists led by researchers at the University of Massachusetts Medical School (UMMS). Mutations to the profilin (PFN1) gene, which is essential to the growth and development of nerve cell axons, is estimated to account for one to two percent of inherited ALS cases. The finding, described today in the online edition of Nature, points to defects in a neuron's cytoskeleton structure as a potential common feature among diverse ALS genes.

"This discovery identifies what may possibly be a common biological mechanism involved across familial ALS cases regardless of genetics," said John Landers, PhD, associate professor of neurology and senior author of the study. "We know of at least three other ALS genes, in addition to PFN1, that adversely impact axon growth. If indeed, this is part of the disease's mechanism, then it might also be a potential target for therapeutics."

Robert Brown, MD, DPhil, a co-author on the study and chair of neurology at UMass Medical School, said "Dr. Landers has done great work in defining this new pathway for motor neuron death. We are delighted to have identified the defects in families from the U.S., Israel and France that we have been investigating for several years. Our finding is particularly exciting because it may provide new insights into ALS treatment targets."

ALS is a progressive, neurodegenerative disorder affecting the motor neurons in the central nervous system. As motor neurons die, the brain's ability to send signals to the body's muscles is compromised. This leads to loss of voluntary muscle movement, paralysis and eventually respiratory failure. The cause of most cases of ALS is not known. Approximately 10 percent of cases are inherited. Though investigators at UMass Medical School and elsewhere have identified several genes shown to cause inherited or familial ALS, almost 50 percent of these cases have an unknown genetic cause.

The current Nature study details the discovery of the PFN1 gene mutation among two large ALS families. Both families were negative for known ALS-causing mutations and displayed familial relationships that suggested a dominant inheritance mode for the disease. For each family, two affected members with maximum genetic distance were selected for deep DNA sequencing. To identify an ALS-causing mutation, genetic variations between the family members were identified and screened against known databases of human genetic variation, such as the 1000 Genomes Project. This narrowed down the resulting number of candidate, ALS-causing mutations to two within the first family and three within the second. Interestingly, both families contained different mutations within the same gene PFN1, the likely causative mutation. With additional screening, the team documented that in a total of 274 families sequenced, seven contained a mutation to the PFN1 gene, establishing it as a likely cause for ALS.

While it is not certain how the PFN1 mutation causes ALS, the cellular functions it controls within the motor neurons are responsible for regulation of a number of activities, including the growth and development of the axon, the slender projection through which neurons transmit electrical impulses to neighboring cells, such as muscle. When introduced into motor neuron cells, normal PFN1 protein was found diffused throughout the cytoplasm. Conversely, the mutant PFN1 observed in ALS patients was found to collect in dense aggregates, keeping it from functioning properly. Motor neurons producing mutated PFN1 showed markedly shorter axon outgrowth.

"The discovery that mutant PFN1 interferes with axon outgrowth was very exciting to us," said Claudia Fallini, PhD, a postdoctoral researcher at Emory University School of Medicine who collaborated with the UMass Medical School authors to investigate PFN1's functions in cultured motor neurons. "It suggests that alterations in actin dynamics may be an important mechanism at the basis of motor neuron degeneration."

"In healthy neurons, PFN1 acts almost like a railroad tie for fibrous filaments called actin, which make up the axon" said Landers. "PFN1 helps bind these filaments to each other, promoting outgrowth of the axon. Without properly functioning PFN1 these filaments can't come together. Here we show that mutant PFN1 may contribute to ALS pathogeneses by accumulating in these aggregates and altering the actin dynamics in a way that inhibits axon outgrowth."

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UMMS researchers isolate gene mutations in patients with inherited amyotrophic lateral sclerosis

New brain scans to be used to treat people before symptoms of mental decline.

TWO decades ago, researchers began discovering rare gene mutations that cause Alzheimer's disease in all who inherit them. Now, they have found the opposite: a mutation that prevents the devastating brain disorder. The protective mutation also is very rare - it is not the reason most people do not develop Alzheimer's disease.

But what intrigues researchers is how it protects the brain. It does the reverse of what the mutations that cause Alzheimer's do. Those mutations lead to excessive amounts of a normal substance, beta amyloid, in the brain. The protective mutation slows beta amyloid production, so people make much less.

The discovery, published online in the journal Nature, provides strong evidence that beta amyloid build-up is a driving force in this destructive brain disease. It also bolsters the hopes of drug companies that have zealously developed drugs to reduce amyloid levels with the expectation they might alter the course of the disease or even prevent it.

So far, the drugs have not succeeded, but companies and many researchers have argued that there are reasons for that and that it is too soon to give up on them. If for no other reason, the discovery's implication for drug development ''is hugely important'', said Dr David Altshuler, a genomics expert at Harvard Medical School and the Broad Institute of Harvard and MIT who was not involved with the research.

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It indicates, he said, that drug companies' big bets on anti-amyloid treatments could pay off.

''This paper provides strong evidence that it would work in the general population if you did it right,'' Dr Altshuler said.

Dr Samuel Gandy, an Alzheimer's researcher who directs the Mount Sinai Centre for Cognitive Health, had a similar response, calling the finding ''extraordinarily important'' - the most significant in the field since researchers first reported a mutation that leads to the disease, 22 years ago.

The discovery of the protective gene mutation, a product of the revolution that has taken place in genetics, arose when researchers scanned the entire DNA of 1795 Icelanders.

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Rare gene mutation could block Alzheimer's

July 13, 2012

Connie K. Ho for redOrbit.com Your Universe Online

Scientists from the Washington University School of Medicine recently revealed that they have developed a timeline that shows early signs of Alzheimers, even with unseen progress.

The team of researchers examined families who had a genetic risk of having the disease. The findings, which were published recently in the New England Journal of Medicine, show that signs of Alzheimers can appear up to 25 years before diagnosis of the disorder.

This important research highlights that key changes in the brain, linked to the inherited form of Alzheimers disease, happen decades before symptoms show, which may have major implications for diagnosis and treatment in the future, commented Clive Ballard, director of research at the Alzheimers Society, in a article by the BBC.

The study included 128 people from Australia, the United Kingdom, and the United States. Of all the participants, 50 percent had the possibility of inheriting one of three mutations that could lead to Alzheimers. These mutations were found in people who were in their 30s and 40s, and those who had the mutations would later develop Alzheimers. Researchers state that the findings are useful in understanding the patterns leading up to Alzheimers. The patients who had the mutations were much younger than the people with the illness, which normally affects people who are 60 years of age or older.

The ability to detect the very earliest stages of Alzheimers would not only allow people to plan and access care and existing treatments far sooner, but would also enable new drugs to be trialed in the right people, at the right time, noted Dr. Eric Karran, director of Research at Alzheimers Research UK, in the BBC article.

The researchers studied the age at which the subjects parents were when they started to develop the disease to determine the number of years it would take for symptoms of Alzheimers to appear. The subjects participated in blood and spinal fluid tests, brain scans, and exams that tested their mental ability. The scientists determined that the earliest change could be seen 25 years before the onset of the disease.

Overall, these changes in sugar glucose and memory problems were observed 10 years before symptoms materialized. The scientists saw that there was a decrease in the spinal fluid levels related to Alzheimers brain plaques. They also determined that there was shrinkage in parts of the brain along with increases in the levels of tau, a structural protein found in brain cells.

These findings are a good indicator that there may be key changes in the brain happening early in people who develop non-hereditary Alzheimers disease, but we cant be sure. Further research into this complex condition is needed to confirm a definite link, remarked Ballard in the BBC article.

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Researchers Develop Alzheimer’s Timeline

UC Davis' fledgling genetics lab in Sacramento announced its first major research project Thursday, a massive study of the DNA of salmonella and other bacteria linked to foodborne illnesses.

The five-year project could pay economic dividends for the university and the region. Besides boosting the visibility of the 10-month-old lab, it could enhance Sacramento's modest credentials as a life-sciences hub.

"This is a game-changer, and it's happening right there in Sacramento," said Paul Zavitsanos of Agilent Technologies Inc., the $6 billion-a-year Silicon Valley scientific-instrument maker that's helping fund the project.

Researchers plan to sequence, or map, the genes of 100,000 infectious microorganisms. The work, known as the 100K Genome Project, will be done at the new BGI@UCDavis genomics lab, on the university's medical complex in Sacramento.

"It will raise the profile of the BGI@UCDavis facility tremendously," said Bart Weimer, a university veterinarian and co-director of the facility. He said preliminary work on the project actually began in March.

The genetics lab, a collaboration with world-renowned Chinese research institute BGI, employs just three workers, but that will grow. Weimer plans to hire six assistants for the food-safety project alone, and eventually the facility is expected to employ 200 or more workers.

Community leaders hope it could spawn new companies and provide a spark for the region's smallish life-sciences industry, which has struggled to gain traction.

The facility is already showing up on radar screens in the genetics world.

The U.S. Food and Drug Administration, a partner in the food-safety project, said the UC Davis facility was chosen partly because of sheer horsepower. While it took the FDA three years to sequence the genes of 500 strains of salmonella, the Sacramento lab is expected to map 100,000 different pathogens in five years.

"It has a substantial ability to do sequencing," said Steven Musser, director of the FDA's office of regulatory science for food safety.

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UC Davis lab to study bacteria linked to food-borne illnesses

By Ryan Flinn - 2012-07-13T14:02:10Z

Seattle Genetics Inc. (SGEN) Chief Executive Officer Clay Siegall says he has a model for growth of the biotechnology companys only drug, cancer treatment Adcetris: Roche Holding AG (ROG)s $6.7 billion-seller Rituxan.

Adcetris received U.S. clearance in August for use by Hodgkins lymphoma patients who failed on other therapies, a smaller market than the front-line treatment the company aims for after added trials are completed in the next few years. Rituxan, approved as an initial treatment for lymphoma in 1997, took a similar path, Siegall said in a telephone interview.

Analysts expect Adcetris to reach $437 million in sales in 2015, the average of three estimates in a Bloomberg survey. The drugs prospects have boosted the companys shares by 52 percent this year through yesterday, giving the company a market value of almost $3 billion. That potential also makes Seattle Genetics less likely to seek a merger or be acquired now, Siegall said.

Adcetris is a very important brand, and can become a $1 billion brand in a number of years, Siegall said. The drugmaker has great trajectory going forward, so its not a time where we feel that its right for the company to get sold or flipped.

Seattle Genetics fell less than 1 percent to $25.30 at 9:58 a.m. New York time.

Adcetris combines a cancer-targeting antibody with the cell-killing effects of chemotherapy. The drug, known chemically as brentuximab, is Seattle Genetics first product, and was also cleared by regulators to treat patients with a rarer cancer known as systemic anaplastic large cell lymphoma or ALCL, who had also failed previous treatments.

Hodgkins lymphoma will be diagnosed in an estimated 9,060 U.S. patients this year and will cause the death of about 1,190 people, according to the National Cancer Institute in Bethesda, Maryland. The disease begins in the white-blood cells and most commonly strikes people from ages 15 to 35 and older than 55.

Roches Genentech unit also initially got approved in one type of low-grade lymphoma, and then got approved in a variety of different aggressive and high grade lymphomas, and even some other non-lymphomas, Siegall said.

Half of the 14 analysts in a Bloomberg survey recommend purchasing Seattle Genetics shares, with three rating them a sell.

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Seattle Genetics CEO Says Drug Growth Path Means No Sale

Gene-Silencing Technique Targets Scarring

A biotech company founded by Craig Mello, codiscoverer of RNAi, brings its first self-delivering interfering RNA to clinical trial.

A clinical trial of a gene-silencing treatment for reducing excessive scarring is now underway, bringing the number of active clinical trials for the as-yet-unproven gene-silencing process known as RNA interference to nearly 20.

Massachusetts-based RXi Pharmaceuticals has developed a chemically modified version of the small interfering RNAs that drive the biochemical process of RNA interference, or RNAi.

RNAi was discovered in 1998 and has since exploded as a research tool for turning off genes of choice in lab settings. Soon thereafter, biotech and pharmaceutical companies turned their attention to siRNAsshort pieces of RNA, DNA's cousin, that can prevent the activity of the specific gene they complementas a potential therapeutic tool, but so far no one has successfully commercialized the technology. The technology holds the potential to reduce the effects of almost any gene in a human cell, if only the interfering RNAs can get inside.

"Because RNA does not normally pass through the membrane of the cell, that delivery step is a major challenge," says Phil Sharp, a molecular biologist at MIT and a cofounder of an RNAi company called Alynylam (Sharp previously discussed the therapeutic potential of RNAi with Technology Review). Researchers must also strike a balance between the potency of the therapy in targeted cells and side-effects in other cells, he says.

A skin treatment reduces some of the delivery challenge because the target area is easily accessible. RXi injects its scar therapy directly under the outermost layers of the skin, delivering a large amount of the treatment to the target area, thereby reducing the risk of side effects to other parts of the body.

On a molecular level, the company modifies its interfering RNAs so that they are absorbed by the membrane of a cell. The company adds cholesterol molecules, which are normal components of cell membranes, to the RNAs so that the molecule will be more readily absorbed. Once in the membrane, the cholesterol breaks from the RNA molecule, which can then enter the cell body. RXi's version of siRNAs are also shorter than conventional siRNAs and have been chemically modified to resist the enzymatic wear and tear inside cells.

The scar-treating compound was designed to reduce the expression of a protein called connective tissue growth factor, or CTGF, which regulates several biological pathways involved in wound healing and scar formation. The protein drives production of collagen and other cellular support molecules referred to as matrix proteins.

In some people, CTGF overproduces these components, resulting in excessive scarring such as raised scars or larges scars called keloids. RXi's CEO Geert Cauwenbergh says the company's interfering RNA reduces scaring while still allowing CTGF to perform its wound-healing properties. "The interfering RNA doesn't silence [CTGF] 100 percentit continues to have some effect, but it's not excessive," he says.

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Gene-Silencing Technique Targets Scarring

July 12, 2012

By Christy Lewis

MEDFORD, Ore. -- After years of fighting Alzheimer's disease, researchers spotted a gene that could change the future of Alzheimer's treatment.

Here are the basics of it all: researchers found a rare gene mutation that protects and stops the build up of a protein called beta amyloid. The production of the amyloids has been a possible cause for the disease, but this new discovery confirms that idea.

Not only does this discovery demonstrate a way to slow the symptoms of Alzheimer's, but it also verifies everything researchers have been working on. It means they're moving in the right direction toward better Alzheimer's treatment.

The gene could potentially lead to successfully preventing the disease or slowing down the production of the amyloid proteins. But the discovery doesn't provide help for those who already suffer from the disease right now.

Researchers say it could be years before anyone reaps the benefits of this discovery, but it certainly provides a positive outlook down the road for folks who'll likely get the disease.

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Alzheimer's Research Uncovers New Gene Mutation

That painful sunburn is actually a complex volley of genetically encoded counterattacks buried deep under your skin.

The sun is scorching your RNA, says a study published in Nature Medicine.

In some ways, it was a surprise. said Dr. Richard Gallo, chief of the dermatology division at the University of California San Diego. We know a sunburn will damage DNA. What we didnt suspect is that it is also damaging the RNA.

DNA stores genetic code; RNA transmits it.

The study found that ultraviolet UVB rays from the sun bore through the skin to fracture and tangle a specific type of RNA that does not make proteins.

Sunburned cells release that noncoding micro-RNA, setting off an alarm in healthy surrounding cells that something weird and dangerous is going on.

That alarm turns into inflammation, which turns into sunburn.

We were interested in how the injury is recognized by our body, Gallo said. Those cells that are injured are dead. How can their neighbours detect that?

In fact, the inflammation is the skin trying to heal itself, releasing a cocktail of antibodies and anti-inflammatories that could be beneficial.

It may help us remove cells that might otherwise turn into skin cancer.

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Science of sunburn reveals it damages both DNA and RNA

Some drugs in development target what scientists have thought is the root cause of Alzheimer's - the buildup in the brain of amyloid protein. Newly published research supports such treatments.

Researchers have discovered for the first time a genetic mutation that may protect people against the degenerative brain disease that affects almost 30 million people worldwide.

Results from key Alzheimer's studies could decide future of treatment Watch: An Alzheimer's researcher who is also a patient

In the U.S. there's about 5.4 million people with the disease, but barring a medical breakthrough, researchers estimate by 2050 that the number of people with Alzheimer's will grow to 16 million.

For the new research, published in the July 11 issue of Nature, a team of scientists from Iceland took a closer look at what's called amyloid-beta precursor protein (APP).

APP was discovered about 25 years ago in patients with rare inherited forms of Alzheimer's that is developed in middle age, reports Nature News. According to the researchers, APP breaks down into amyloid-beta, which shows up as plaques in the brain that are a telltale marker of the disease. Scientists have debated whether the plaque buildup contributes to causing the disease or is caused by Alzheimer's.

The scientists in the new study compared the complete genome sequences of nearly 1,800 elderly Icelanders with their medical histories and discovered a genetic mutation in a gene that produces APP. The mutation was found to slow plaque formation in the brain by 40 percent.

Looking for the mutation in 400,000 Scandinavians, the researchers estimated that people who possess the mutation are more than five times as likely to reach 85 without developing Alzheimer's disease. People without Alzheimer's who had the mutation were also less likely to experience cognitive decline that comes with aging, suggesting that memory loss with aging and Alzheimer's disease may share a root cause.

"Pathologists have always suspected that there was a substantial overlap between Alzheimer's disease and normal age-related changes," study author Kri Stefnsson, chief executive of deCODE Genetics in Reykjavik, Iceland, told Nature News.

Since drug companies are currently investigating drugs that target amyloid production, as CBS This Morning reported in May, the new study may come as a sigh of relief for many scientists.

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Genetic mutation may protect against Alzheimer's

Alzheimer's, Dementia & Mental Health

Game-Changing Find in Battle Against Alzheimers: A Gene Offers Protection

Study links cognitive decline in senior citizens with Alzheimers disease; says amyloid-beta plaque is cause of AD

July 12, 2012 - New research by deCODE Genetics is a game-changer in the battle against Alzheimers disease. It reveals a gene that protects against Alzheimers disease (AD) and even cognitive decline in the elderly. The discovery also finds linkage between age-related cognitive decline and late-onset forms of AD, the most common cause of dementia.

The gene that protects against AD is a variant of the amyloid precursor protein (APP) gene.

APP was discovered 25 years ago in patients with rare, inherited forms of Alzheimers that strike in middle age, writes Ewen Callaway in a news report in the journal Nature, which reported the research.

Related Stories at SeniorJournal.com

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Game-Changing Find in Battle Against Alzheimer’s: A Gene Offers Protection

UC Davis today announced a major genetics research project to be carried out at its new gene laboratory in Sacramento.

The study, involving the DNA of 100,000 infectious microorganisms, is one of the first major projects to be undertaken at the nine-month-old BGI@UCDavis genome lab.

The lab is a much-ballyhooed partnership with BGI, a Chinese research institute. The DNA lab, which was announced last fall, is expected to create 200 jobs and invigorate the Sacramento area's tech sector.

Under the five-year project announced today, Davis researchers will work with Silicon Valley's Agilent Technologies and three federal agencies: the Food and Drug Administration, Centers for Disease Control and Prevention and Department of Agriculture.

The idea behind the project is to improve food safety and develop new diagnostic tools. Researchers at the lab, located at the School of Medicine in Sacramento, will examine pathogens such as salmonella, listeria and e. coli.

"This landmark project harnesses UC Davis' partnership with BGI, a world leader in genomics, to mine information about the most deadly foodborne pathogens," said the university's vice chancellor for research Harris Lewin in a press release. "It will revolutionize our basic understanding of these disease-causing microorganisms."

Agilent is contributing several hundred thousand dollars in funding. In return, it will get an advance look at the fruits of the research, which will eventually be made public.

"This is huge, this is a really big deal," said Paul Zavitsanos, manager of global food safety at Agilent.

He said Agilent had already been working on food-safety issues at Davis' veterinary school and Robert Mondavi Institute for Wine and Food Science. Conducting research at the DNA lab is "a logical extension," he said.

The federal agencies will contribute various bacterial strains to the project.

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UC Davis announces major research project at new gene lab

Public release date: 12-Jul-2012 [ | E-mail | Share ]

Contact: Cathia Falvey cfalvey@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, July 12, 2012The profound sense of loss and public mourning that followed the death of Apple co-founder Steve Jobs was a reflection of how great an impact he had on society and on the lives of individuals through the technology he helped to create. The magnitude and reasons for the outpouring of emotion upon his death by people who did not know him personally are explored in an article in Cyberpsychology, Behavior, and Social Networking, a peer-reviewed journal published by Mary Ann Liebert, Inc., publishers (http://www.liebertpub.com). The article is available free online at the Cyberpsychology, Behavior, and Social Networking (http://www.liebertpub.com/cyber) website.

"Steve Jobs touched so many people because he dared to be different, he was unconventional, he was brilliant, and that, combined with his uncompromising nature, resulted in a company whose products had no peer," says Mary Ann Liebert, CEO and Publisher. "Very few of us know anyone like that personally, and when he died, a hero and a magician was gone."

"We'll Miss You Steve: How the Death of a Technology Innovator Emotionally Impacts Those Who Use and Love his Digital Devices (http://online.liebertpub.com/doi/full/10.1089/cyber.2011.0623)," reviews three studies that explore people's emotional connections to technology and even to a particular device and how that relationship may extend beyond the technology to feelings of personal connectedness and loss when the relationship ends.

Andrew Przybylski, University of Essex, Colchester, U.K., compares and discusses the findings of studies conducted during the weeks following Steve Jobs' death in October 2011. The studies evaluated the types of people most likely to be emotionally impacted and how their psychological link to Apple devices relates to their sadness and overall response to Jobs' passing.

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About the Journal

Cyberpsychology, Behavior, and Social Networking (http://www.liebertpub.com/cyber) is an authoritative peer-reviewed journal published monthly in print and online that explores the psychological and social issues surrounding the Internet and interactive technologies. Complete tables of content and a sample issue may be viewed online at the Cyberpsychology, Behavior, and Social Networking (http://www.liebertpub.com/cyber) website.

About the Publisher

Continued here:
Why did Steve Job's death affect people who never knew him?

SAN DIEGO, July 12, 2012 /PRNewswire/ --Sequenom, Inc. (SQNM), a life sciences company providing innovative genetic analysis solutions, today announced it will report financial results for the second quarter 2012 after closing of the NASDAQ Global Market on Thursday, July 26, 2012.

A conference call hosted by Harry F. Hixson, Jr., Ph.D., Chairman and CEO, and other members of senior management will take place on the same day at 5:00pm ET (2:00pm PT) and will be webcast live on the Sequenom website.

To access the live teleconference call, dial 800-860-2442 in the U.S., 866-605-3852 in Canada (both are toll free), and 412-858-4600 for other international callers. Please specify to the operator that you would like to join the "Sequenom Second Quarter 2012 Earnings Conference Call." If you are unable to listen to the live webcast, a teleconference replay will be available through Friday, August 3, 2012. Interested parties can access the rebroadcast by dialing 877-344-7529 or 412-317-0088 internationally and entering the conference number 10016291.

The conference call webcast is accessible through the "Investors" section of the Sequenom website at http://ir.sequenom.com. An online replay will be available following the initial broadcast until Thursday, August 2, 2012.

About Sequenom

Sequenom, Inc. (SQNM) is a life sciences company committed to improving healthcare through revolutionary genetic analysis solutions. Sequenom develops innovative technology, products and diagnostic tests that target and serve discovery and clinical research, and molecular diagnostics markets. The company was founded in 1994 and is headquartered in San Diego, California. Sequenom maintains a Web site at http://www.sequenom.com to which Sequenom regularly posts copies of its press releases as well as additional information about Sequenom. Interested persons can subscribe on the Sequenom Web site to email alerts or RSS feeds that are sent automatically when Sequenom issues press releases, files its reports with the Securities and Exchange Commission or posts certain other information to the Web site.

About Sequenom Center for Molecular Medicine

Sequenom Center for Molecular Medicine (Sequenom CMM) has two CAP accredited and CLIA-certified molecular diagnostics reference laboratories dedicated to the development and commercialization of laboratory developed tests for prenatal and eye conditions and diseases. Utilizing innovative proprietary technologies, Sequenom CMM provides test results that can be used as tools by clinicians in managing patient care. Testing services are available only upon request to physicians. Sequenom CMM works closely with key opinion leaders and experts in obstetrics, retinal care and genetics. Sequenom CMM scientists use a variety of sophisticated and cutting-edge methodologies in the development and validation of tests. Sequenom CMM is changing the landscape in genetic diagnostics. Visit http://www.scmmlab.com for more information on laboratory testing services.

SEQUENOM, MaterniT21 and MaterniT21 PLUS are trademarks of Sequenom. All other trademarks and service marks are the property of their respective owners.

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Sequenom, Inc. Announces Date Of Second Quarter 2012 Financial Results And Conference Call

Public release date: 12-Jul-2012 [ | E-mail | Share ]

Contact: Cathia Falvey cfalvey@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, July 12, 2012 Although acetazolamide is widely prescribed to prevent and treat acute mountain sickness (AMS), the appropriate dose at which it is effective and safe has not been clearly defined. A comprehensive review and meta-analysis of 24 studies comparing the efficacy and risks associated with increasing doses of acetazolamide is published in High Altitude Medicine & Biology, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers (http://www.liebertpub.com). The article is available free online at the High Altitude Medicine & Biology (http://www.liebertpub.com/ham) website.

Bengt Kayser and colleagues, University of Geneva, Switzerland, reviewed the data compiled on more than 1,000 subjects and describe the relationship between efficacy in preventing and treating AMS, risk of side effects, and increasing drug dosages. They discuss their findings in the article "Reappraisal of Acetazolamide for the Prevention of Acute Mountain Sickness: A Systematic Review and Meta-Analysis (http://online.liebertpub.com/doi/full/10.1089/ham.2011.1084)."

Unless the baseline risk of AMS is high, as with rapid transport to high altitude (as opposed to a slow ascent), acetazolamide has limited effectiveness. Some side effects occur with even the lowest doses of the drug, whereas others appear to be dose-dependent. The authors suggest that treatment be tailored for the individual depending on AMS risk and acceptability of the most common side effects such as increased urination, numbness and tingling, and taste disturbance.

"This is a valuable contribution on the pros and cons of using the most important medication for preventing and treating acute mountain sickness," says John B. West, MD, PhD, Editor-in-Chief of High Altitude Medicine & Biology and Professor of Medicine at the University of California, San Diego School of Medicine.

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About the Journal

High Altitude Medicine & Biology (http://www.liebertpub.com/ham), the Official Journal of the International Society for Mountain Medicine (http://www.ismmed.org/), is published quarterly online. It is the only peer-reviewed journal dedicated exclusively to the latest advances in high altitude life sciences. The journal presents findings on the effects of chronic hypoxia on lung and heart disease, pulmonary and cerebral edema, hypertension, dehydration, infertility, appetite and weight loss, and other diseases. Complete tables of content and sample issue may be viewed online at the High Altitude Medicine & Biology (http://www.liebertpub.com/ham) website.

About the Publisher

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Is acetazolamide effective and safe for preventing acute mountain sickness?

Every investor would love to stumble upon the perfect stock. But will you ever really find a stock that provides everything you could possibly want?

One thing's for sure: You'll never discover truly great investments unless you actively look for them. Let's discuss the ideal qualities of a perfect stock, then decide if Seattle Genetics (Nasdaq: SGEN) fits the bill.

The quest for perfectionStocks that look great based on one factor may prove horrible elsewhere, making due diligence a crucial part of your investing research. The best stocks excel in many different areas, including these important factors:

With those factors in mind, let's take a closer look at Seattle Genetics.

Factor

What We Want to See

Actual

Pass or Fail?

Source: S&P Capital IQ. NM = not meaningful due to negative earnings. Total score = number of passes.

Since we looked at Seattle Genetics last year, the company has picked up a point. Revenue is now back moving in the right direction, but even though the shares are up almost 30% over the past year, the biotech still isn't making a profit.

See the article here:
Has Seattle Genetics Become the Perfect Stock?

A close examination ofemerging biotech Pluristem Therapeutics (PSTI), whose unique cell therapy is being applied to a number of clinical disorders, shows promise.

Peripheral arterial disease (PAD), under-diagnosed and, in some cases, over-treated, is one of the fastest-growing conditions to affect an aging population. 10 million Americans have PAD today and the number is expected to rise to 23 million by 2014. Its presence signals circulatory problems that play into medicine`s largest industries - heart disease and stroke. We believe the market is ready for a new treatment, cell therapy, with lower overall cost, quicker healing time, no toxicity, and ease of administration - a simple intramuscular injection - to help improve the PAD sufferers` way of life.

Several big pharmas sell drugs for PAD including Bristol-Myers Sqibb Co. (BMY) and Sanofi (SNY) which sell Plavix; Teva Pharmaceuticals (TEVA) sells Pletal; AstraZeneca (AZN) sells Atacand; Bristol-Myers also sells Avapro; and Merck & Co. (MRK) sell Cozaar/Hyzaar. Combined sales for these drugs are well over $12 billion. Each of the drugs has side effects and they do not cure PAD. As an alternative, or in addition to drugs, cevices such as stents are surgeries are costly, risky, and not consistently effective.

Pluristem`s PLX cells offer a new paradigm to treat PAD by growing new vessels - offering a potential cure, not just a way to manage the disease.

Peripheral arterial disease (PAD), , is a vascular disease affecting the legs. Its cause is atherosclerosis, where blood flow within arteries becomes restricted from blood-borne debris, allowing plaque to form that narrows and hardens the vessel wall. The first indication of PAD is walking pain, known as intermittent claudication (IC). Left untreated, blood flow to the legs is further limited, resulting in critical leg ischemia (CLI), or dying arterial tissue; almost half of PAD patients with IC progress to CLI. At this point, ulcers and gangrene may develop with amputation as the only option.

Two goals are targeted when treating PAD: managing leg pain and halting the progression of atherosclerosis, which, when present, may be a signal that its appearance is elsewhere in the body, raising the risk of heart attack and stroke. Often doctors suggest combining medicine for PAD with procedural intervention. In severe cases, vascular surgery is recommended.

Pharmaceutical treatment for PAD falls in two major categories - drugs that improve blood flow and those that thin blood to avoid excessive clotting that intensifies atherosclerosis. Aspirin, coumadin, and heparin have been standards of care as anti-clotting agents that inhibit platelets, small cell fragments that circulate in blood, from forming clots.

Then came clopidogrel, or Plavix, made and sold by Bristol-Myers Sqibb Co. (BMY) and Sanofi (SNY). It works by inhibiting a receptor on platelet cell membranes so they become less `sticky` and clots are less likely to form. The drug quickly rose to blockbuster status and is today the second most prescribed pharmaceutical in the U.S., next to anti-cholesterol agent Lipitor, marketed by Pfizer, Inc. (PFE). Sales of Plavix were $7.1 billion in 2011, up 6% over the prior year, and accounted for 33% of Bristol-Myers` net revenue. Treatment with Plavix is lifelong.

Bestseller Plavix`s Surprising Drug Interactions and Alarming Side Effects

But there are problems with Plavix. Two years ago, the FDA put a `black box` warning on the popular drug, citing a lack of efficacy in an astounding 14% of patients. It was discovered that people with certain genetic characteristics simply cannot metabolize the drug, rendering it useless in the body. Sadly, the patient would need to take Plavix over time before it is determined that it doesn`t work, setting up a scenario of further arterial blockage. The only solution is a genetic test given either before or after administration of the drug - at price of $500 - and a wait time of two weeks.

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Pluristem's Unique Therapy Primed to Replace Blockbuster Drugs for Treating Peripheral Arterial Disease

Results Provide Boost for Drugs in the Pipeline Targeting the Gene

July 11, 2012 -- Can Alzheimer's disease be prevented?

A new study shows that researchers might be on the right path to someday make it happen. New research has identified a genetic mutation that may protect against both Alzheimer's disease and age-related declines in thinking and memory. And future drug treatments already in the pipeline may help prevent against both.

Amyloid protein plaques in the brain are seen in people with Alzheimer's disease. A gene for amyloid-beta precursor protein (APP) plays a key role in the formation of these plaques. Researchers from Reykjavik, Iceland, found that a mutation in this gene may help protect against Alzheimer's disease and age-related mental decline.

This mutation is rare, but, when present, confers about a 40% reduction in amyloid plaque-forming proteins. What's more, study participants between 80 to 100 years old without Alzheimer's disease who carry this mutation have better mental function than those without the mutation, the study shows.

The findings appear in Nature.

Alzheimer's disease affects memory and thinking. Symptoms usually develop slowly and worsen with time. One in eight older Americans has Alzheimer's disease, making it the most common type of dementia in the U.S., according to the Alzheimer's Association.

U.S. Alzheimer's disease researchers are enthused about the new findings and what they may mean for prevention.

"This is an extraordinary paper," Sam Gandy, MD, PhD, says in an email. He is the Mount Sinai chair in Alzheimer's disease research at Mount Sinai School of Medicine in New York City. "This provides some of the strongest evidence ever that amyloid is the right target in Alzheimer's."

Many researchers are developing treatments that target amyloid protein. "Amyloid researchers the world over couldn't have asked for a better morale booster," he says. "This is a great gift to those at high risk for future development of Alzheimer's disease because this means our prevention trials are aiming at the right target."

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Gene May Protect Against Alzheimer’s Disease

Public release date: 11-Jul-2012 [ | E-mail | Share ]

Contact: Cathia Falvey cfalvey@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, July 11, 2012As athletes from around the world compete for medals at the Summer Olympics in London, the city will be striving to meet Olympic-level sustainability goals. A fascinating first-person view of how these sustainability targets were developed and will be achieved is featured in Sustainability: The Journal of Record, a publication of Mary Ann Liebert, Inc., publishers (www.liebertpub.com) The article is available free online at the Sustainability: The Journal of Record (www.liebertpub.com/sus) website.

The central location of the Summer 2012 Olympics is the East End neighborhood of Stratford, once known as an industrial wasteland. But it has been transformed into a model for sustainability, developed under the guidance of five key themes: climate change, waste, biodiversity, inclusion, and healthy living. The use of public transportation only on the Olympic groundsno cars permitted and no parking lotsis just one example of the extent to which London has gone to reach its sustainability goals. Another example: no waste will flow directly to landfills, through a combined effort involving composting, recycling, and reduced packaging use.

Shaun McCarthy, Chair of the Commission for a Sustainable London, the independent watchdog group responsible for making sure sustainability goals for the Summer Games are tracked and met, discusses the challenges and the progress being made as the Games approach in the article entitled, "The Olympics Go for the Green: With the 2012 Games Looming, London Works to Raise Bar in Sustainability (http://online.liebertpub.com/doi/pdfplus/10.1089/SUS.2012.9965)."

"The Olympic Games are the singular event of our time where the whole world will be watching, and to have sustainability be such a visible factor in the Games is invaluable to the sustainability movement," says Jamie Devereaux, Editor of Sustainability: The Journal of Record (www.liebertpub.com/sus).

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About the Journal

Sustainability: The Journal of Record (www.liebertpub.com/sus) documents the implementation of sustainability programs in higher education and business, and provides the central forum for academic institutions, the business community, foundations, government agencies, and leaders of green-collar endeavors to share and learn about one another's progress and programs. The Journal fosters collaborations among all stakeholders for attaining mutually supportive objectives. Complete tables of content and a sample issue may be viewed online at the Sustainability: The Journal of Record (www.liebertpub.com/sus) website.

About the Publisher

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Summer Olympics go for the green as London prepares to host the world

That painful sunburn on your shoulder is actually a complex volley of genetically encoded counterattacks buried deep under your skin.

According to a study published in Medicine, the sun is scorching your RNA.

In some ways, it was a surprise, said Dr. Richard Gallo, chief of the dermatology division at the University of California San Diego. We know a sunburn will damage DNA. What we didnt suspect is that it is also damaging the RNA.

DNA stores genetic code; RNA transmits it.

The study found that ultraviolet UVB rays from the sun bore through the skin to fracture and tangle a specific type of RNA that does not make proteins. Sunburned cells release that non-coding micro-RNA, setting off an alarm in healthy surrounding cells that something weird and dangerous is going on.

That alarm turns into inflammation which turns into sunburn

We were interested in how the injury is recognized by our body, Gallo said on Monday. Those cells that are injured are dead. How can their neighbours detect that?

In fact, the inflammation is the skin trying to heal itself, releasing a cocktail of antibodies and anti-inflammatories that could be beneficial.

It may help us remove cells that might otherwise turn into skin cancer.

Scientists sequenced all of the RNA in human and mouse cells used in the study that were exposed to ultraviolet light to figure out which molecules reacted in which way to a dose of too much sun.

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Break out the sunscreen: Sunburns damage your genetic code

Traditionally, undergraduate-level genetics courses begin with Mendel and his peas, and then move on to other concepts in roughly the same order in which they were discovered. But such an approach is increasingly considered outdated.

In a PLoS Biology opinion piece, the University of British Columbia's Rosie Redfield recounts her department's revamping of the conventional intro genetics course. Rather than following the historical approach, the new UBC course instead starts with coursework on gene function and inheritance before getting to genetic analysis. However, Redfield says, these changes aren't enough. "Our goal in designing the course had been to make students competent in the standard principles of transmission genetics, but we had totally failed to consider whether this is really what our students need to know," she writes in PLoS Biology.

Redfield suggests a very different approach: crafting a syllabus that begins with personal genomics followed by teachings on the structures and functions of genes and chromosomes, and later followed by historical genetic analyses including those by Mendel. "As a first step, geneticists need to step back from the current curriculum and decide what 21st century students really need to know about genes and inheritance," she writes. "These decisions should be based on how students will use what they learn, and not on what we as geneticists value. Then we can develop specific learning goals."

HT: The Beast, the Bard and the Bot

The rest is here:
Sorry, Mendel

Editor's Choice Main Category: Genetics Also Included In: Psychology / Psychiatry;Pediatrics / Children's Health Article Date: 11 Jul 2012 - 14:00 PDT

Current ratings for: Academic Success Determined By Genetics

The study is published in the July edition of the American Psychological Association's journal Developmental Psychology.

Leading author Kevin Beaver, a professor at the College of Criminology and Criminal Justice at Florida State University explains: "Being able to show that specific genes are related in any way to academic achievement is a big step forward in understanding the developmental pathways among young people."

Beaver and his team discovered three genes in their study, which were identified as DAT1, DRD2 and DRD4 genes, were associated with behaviors, including motivation, intelligence, attention regulation, violence and cognitive skills.

Beaver remarks that although earlier studies have investigated the genetic foundations of intelligence, none of these studies has examined genes that could potentially contribute to educational attainment in population samples.

The team analyzed data from 1,674 respondents obtained from the National Longitudinal Study of Adolescent Health (Add Health), which is a 4-wave study of a nationally representative sample of American adolescents enrolled in 1994 and 1995 when the youths were in middle or high school. The study ended in 2008, when the majority of the respondents were between 24 and 32 years old. All study participants, including their parents were surveyed and interviewed and provided DNA samples.

The genes discovered by the team are known as dopamine transporter and receptor genes, and although every person possesses the DAT1, DRD2 and DRD4 gene, Beaver says that the area of interest lies in the alleles, i.e. the molecular differences within the genes. The researchers found that people with certain alleles within these genes achieved the highest levels of education.

The team explains that dopamine transporter genes help in the production of proteins that control dopamine levels (a neurotransmitter) in the brain, while dopamine receptor genes play a role in neurotransmission. According to earlier studies, dopamine levels are involved in controlling impulsive behavior, attention and intelligence.

The team observed that possessing these alleles alone provided no guarantee of a person going on to higher levels of education, given that lower levels of education were more strongly linked to lower IQ levels, and that regardless of genetic effects, living in poor circumstances and 'mixing up with the wrong people' also led to lower levels of education.

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Academic Success Determined By Genetics