Archive for May, 2014

The Sims 3 Perfect Genetics (Part 3) Relaxing Day!
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The Sims 3 Perfect Genetics (Part 3) Relaxing Day! - Video

Is it Genetics or Just How You Were Raised?
http://www.ihealthtube.com http://www.facebook.com/ihealthtube If you get conditions similar to your parents or grandparents, is it because you were genetica...

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Is it Genetics or Just How You Were Raised? - Video

MSU AgBioResearch: Potato Breeding, Genetics Storage
Scientists at MSU AgBioResearch #39;s Montcalm Research Center are studying potato breeding and genetics, variety development and storage usage for the potato ch...

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MSU AgBioResearch: Potato Breeding, Genetics & Storage - Video

How To Build BIGGER Arms For *YOUR* Genetics (Part 2: Bigger Triceps)
LIKE - SHARE - SUBSCRIBE *** PLEASE NOTE: Contains mature language. Tired of the #39;one-size-fits-all #39; approach to building your arms? NO DOUBT! You may NOT be optimizing your routine...

By: Cory McCarthy

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How To Build BIGGER Arms For *YOUR* Genetics (Part 2: Bigger Triceps) - Video

Minecraft: Think #39;s Lab - Cloning Kopi #39;s DNA - Advanced Genetics Mod Showcase
Subscribe to my Channel: http://bit.ly/NoodleOn Today, Kevin and I work together to push the boundaries of DNA science to find a way to make a clone of Kopi that can make...

By: Thinknoodles

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Minecraft: Think's Lab - Cloning Kopi's DNA - Advanced Genetics Mod Showcase - Video

Gene Delivery System (In-vivo and Ex-vivo) HD
The choice of gene delivery system is very important in the success rate of gene therapy...an assignment solely made for course subject SQG 4143 of Faculty of Biosciences and Medical Engineering...

By: Victoria Ong

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Gene Delivery System (In-vivo and Ex-vivo) HD - Video

AGRC1020 Video Presentation Gene Therapy restores colour vision in monkeys
Presented by Amanda Findlay.

By: Amanda Findlay

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AGRC1020 Video Presentation Gene Therapy restores colour vision in monkeys - Video

Gene therapy for blindness (2012)
Gene Therapy for Retinal Disease Professor Robert MacLaren talks about an exciting new technique for treating a hereditary form of blindness.

By: oxford

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Gene therapy for blindness (2012) - Video

(PRWEB UK) 9 May 2014

Over the course of the human life span the body ages and becomes less able to repair itself, allowing it to become more prone to disease and illness. In the ever developing field of scientific discovery researchers have become intrigued with the concept of finding a way to slow down age-related diseases and prolonging life through the use of medicine. Since the Japanese scientist Shinya Yamanaka (http://bit.ly/1kWb20u) first discovered iPS cells in adult tissue and pioneered mature cell regeneration, this field in medicine has become one of the most rapidly developing fields in biomedicine.

A research team at the National Institute on Ageing at the National Institutes of Health in the US has discovered a promising strategy to arrest ageing by looking at a chemical called SRT1720 which activates a particular protein called Sirtuin 1 (SIRT1). Previous research has demonstrated that activating SIRT1 can have health benefits in various organisms, and it has been proposed as an anti-ageing protein. This study, published in the March edition of Research Journal: Cell (http://bit.ly/1od2gS5) focused on comparing the lifespan, health and diseases of mice fed the same diet, but with or without the addition of a SRT1720.

Overall they found mice fed a normal diet but with the supplement had a longer natural lifespan on average (about five weeks longer). During their lifetime, additional tests also suggested they had improved muscle function and coordination, improved metabolism, improved glucose tolerance, decreased body fat and cholesterol. All in all this suggests that giving the mice this supplement could protect them from the equivalent of metabolic syndrome, a series of risk factors associated with conditions such as heart disease and type 2 diabetes.

A study published today in the journal Stem Cell Reports (http://bit.ly/1hBSDF6) and carried out by the Spanish National Cancer Research Centre's Telomeres and Telomerase Group, reveals that the SIRT1 protein is needed to lengthen and maintain telomeres during cell reprogramming. SIRT1 also guarantees the integrity of the genome of stem cells that come out of the cell reprogramming process; these cells are known as iPS cells (induced Pluripotent Stem cells).

The nature of iPS cells, however, is causing intense debate. The latest research shows that chromosome aberrations and DNA damage can accumulate in these cells. "The problem is that we don't know if these cells are really safe," says Mara Luigia De Bonis, a postdoctoral researcher who has done a large part of the work. http://bit.ly/1m5gRgb

Researchers did not look at whether SIRT1 may cause side effects or complications so it is currently unclear whether SIRT1 would be safe in humans, let alone effective, but this interesting research has opened doors to pharmaceutical companies to develop dietary supplements that can help provide anti-aging pills, especially those who suffer hereditary degenerative diseases. These ongoing scientific studies will help shed light on how cell reprogramming guarantees the healthy functioning of stem cells. This knowledge will help to overcome barriers that come out of the use of iPS cells so they may be used in regenerative medicine.

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Production of synthetic SIRT1 as a dietary supplement may help prolong life, states Chemist Direct

Acute torn meniscus; 5 months after stem cell therapy by Dr Harry Adelson
At Docere Clinics, the vast majority of cases we see are for chronic pain. Occasionally, we get acute injuries and do very well with them. Here, Bryan describes his experience 5 months after...

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Acute torn meniscus; 5 months after stem cell therapy by Dr Harry Adelson - Video

Addiction Rehabilitation Intervention | Personalized Medicine | Russ Scala
Addiction Rehabilitation Treatment | Personalized Medical Health | Russ Scala The Institute #39;s Addiction Rehabilitation program is designed to treat multiple metabolic systems of the body in...

By: Russ Scala

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Addiction Rehabilitation Intervention | Personalized Medicine | Russ Scala - Video

Lokomat Nanos for a Spinal Cord Injury patient in iRehab Physiotherapy Malaysia
A 21-year old incomplete spinal cord injury patient with his first time on the Lokomat Nanos in iRehab Physiotherapy Malaysia.

By: iRehab Physiotherapy

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Lokomat Nanos for a Spinal Cord Injury patient in iRehab Physiotherapy Malaysia - Video

Regenerative Medicine: Making the Impossible Possible
At the Center for Regenerative Medicine, researchers harness Mayo Clinic #39;s collective knowledge, resources and skills to teach your body to heal from within ...

By: Mayo Clinic

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Regenerative Medicine: Making the Impossible Possible - Video

The entire heart muscle in young children may hold untapped potential for regeneration, new research suggests.

For decades, scientists believed that after a child's first few days of life, cardiac muscle cells did not divide. Instead, the assumption was that the heart could only grow by having the muscle cells become larger.

Cracks were already appearing in that theory. But new findings in mice, scheduled for publication in Cell, provide a dramatic counterexample -- with implications for the treatment of congenital heart disorders in humans.

Researchers at Emory University School of Medicine have discovered that in young mice 15 days old, cardiac muscle cells undergo a precisely timed spurt of cell division lasting around a day. The total number of cardiac muscle cells increases by about 40 percent during this time, when the rest of the body is growing rapidly. [A 15-day-old mouse is roughly comparable to a child in kindergarten; puberty occurs at day 30-35 in mice.]

The burst of cell division is driven by a surge of thyroid hormone, the researchers found. This suggests that thyroid hormone could aid in the treatment of children with congenital heart defects. In fact, doctors have already tested thyroid hormone supplementation in this setting on a small scale.

The findings also have broader hints for researchers developing therapies for the heart. Activating the regenerative potential of the muscle cells themselves is a strategy that is an alternative to focusing on the heart's stem cells, says senior author Ahsan Husain, PhD, professor of medicine (cardiology) at Emory University School of Medicine.

"It's not as dramatic as in fish or amphibians, but we can show that in young mice, the entire heart is capable of regeneration, not just the stem cells," he says.

The Emory researchers collaborated with Robert Graham, MD, executive director of the Victor Change Cardiac Research Institute in Australia. Co-first authors of the paper are Nawazish Naqvi, PhD, assistant professor of medicine at Emory and Ming Li, PhD, at Victor Chang.

The researchers tested how much mice, at the age of day 15, can recover from the blockage of a coronary artery. Consistent with previous research, newborn (day 2) mice showed a high level of repair after such an injury, but at day 21, they did not. The day 15 mice recovered more than the day 21 mice, indicating that some repair is still possible at day 15.

The discovery came unexpectedly during the course of Naqvi and Husain's investigation of the role of the gene c-kit -- an important marker for stem cells -- in cardiac muscle growth. Adult mice with a disabled c-kit gene in the heart have more cardiac muscle cells. The researchers wanted to know: when does this difference appear?

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Spurt of heart muscle cell division seen in mice well after birth: Implications for repair of congenital heart defects

Siblings matches traveled from Ethiopia

Behaylu Barry of Stratham, left, poses with his biological sister, Eden, 9, and brother Rediat, 16, both from Ethiopia, at his home in New Hampshire. Eden and Rediat are matches for Behaylus life-saving bone marrow transplant and they will be tested at Boston Childrens Hospital.Deb Cram/dcram@seacoastonline.com

STRATHAM After weeks of anticipation and a roller coaster of emotions, the countdown is on for 13-year-old Behaylu Barry, who is scheduled to undergo a potentially life-saving bone marrow transplant on Monday.

Behaylu was admitted to Boston Children's Hospital last Monday to prepare for the transplant doctors hope will cure his severe aplastic anemia a disease that struck in February and forced his adoptive family from Stratham to scramble to find a bone marrow donor back in his native Ethiopia.

"He's doing very well. He keeps a very strong, positive attitude," said his adoptive father, Aidan Barry.

Behaylu's 16-year-old brother, Rediat Getachew, was a perfect match and will be the donor for the transplant.

Their sister, Eden, 9, was also a match.

Rediat and Eden arrived in New Hampshire on April 22 in anticipation of the transplant. Both live in Ethiopia and had never left their village until word of Behaylu's illness reached them and they provided cheek swabs to see if they were a match for their brother, who was the only child of six to be put up for adoption by his birth parents.

Rediat and Eden were brought to the United States knowing that only one would be selected as the donor.

After an evaluation, Aidan Barry said doctors decided Rediat should be the donor because of his age and size.

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Behaylu Barry's brother to donate bone marrow for transplant

Behaylu Barry's procedure is Monday

Behaylu Barry of Stratham, left, poses with his biological sister, Eden, 9, and brother Rediat, 16, both from Ethiopia, at his home in New Hampshire. Eden and Rediat are matches for Behaylus life-saving bone marrow transplant and they will be tested at Boston Childrens Hospital.Deb Cram/dcram@seacoastonline.com

STRATHAM After weeks of anticipation and a roller coaster of emotions, the countdown is on for 13-year-old Behaylu Barry, who is scheduled to undergo a potentially life-saving bone marrow transplant on Monday.

Behaylu was admitted to Boston Children's Hospital last Monday to prepare for the transplant doctors hope will cure his severe aplastic anemia a disease that struck in February and forced his adoptive family from Stratham to scramble to find a bone marrow donor back in his native Ethiopia.

"He's doing very well. He keeps a very strong, positive attitude," said his adoptive father, Aidan Barry.

Behaylu's 16-year-old brother, Rediat Getachew, was a perfect match and will be the donor for the transplant.

Their sister, Eden, 9, was also a match.

Rediat and Eden arrived in New Hampshire on April 22 in anticipation of the transplant. Both live in Ethiopia and had never left their village until word of Behaylu's illness reached them and they provided cheek swabs to see if they were a match for their brother, who was the only child of six to be put up for adoption by his birth parents.

Rediat and Eden were brought to the United States knowing that only one would be selected as the donor.

After an evaluation, Aidan Barry said doctors decided Rediat should be the donor because of his age and size.

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Boy to receive bone marrow transplant

Eczema is one of the most common skin conditions, affecting up to 30% of people in the US. Symptoms include dry, itchy skin and rashes. But according to new research, having eczema may not be all that bad; it could reduce the risk of skin cancer.

In a study published in the journal eLife, researchers from Kings College London in the UK say that eczema, also known as atopic dermatitis, activates an immune response that sheds potentially cancerous cells from the skin, preventing tumor formation.

According to the research team, including Prof. Fiona Watt of the Centre for Stem Cells and Regenerative Medicine at Kings College, previous studies have suggested that eczema may reduce the risk of skin cancer.

However, they note that this association has proven difficult to confirm in human studies, as medication for eczema may influence cancer risk. Furthermore, symptoms of the condition vary in severity in each individual.

Eczema reduced tumor formation in mice models

For their study, the team genetically engineered mice to have skin defects commonly found in humans with eczema.

They did this by removing structural proteins in the outer layers of their skin, causing them to have an abnormal skin barrier.

The researchers then tested two cancer-causing chemicals in the genetically engineered mice, as well as in normal mice.

They found that the number of benign tumors in defected mice was six times lower than the number found in the normal mice.

Further investigation revealed that although both the defected and normal mice had equal susceptibility to mutations caused by the chemicals, the defected mice had an exaggerated inflammatory response that resulted in potentially cancerous cells being shed from the skin.

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Eczema may reduce skin cancer risk

16 hours ago A signal from Transit-Amplifying Cells (TACs) activates stem cells in the hair follicle, researchers have found. Both types of cells appear in green (top), with TACs clustered lower down. The researchers identified the signal as Sonic Hedgehog. In experiments, such as this one (bottom), they disabled the signal, interfering with hair growth and regeneration.

(Phys.org) Stem cells switch off and on, sometimes dividing to produce progeny cells and sometimes resting. But scientists don't fully understand what causes the cells to toggle between active and quiet states.

New research in Elaine Fuchs' Laboratory of Mammalian Cell Biology and Development focused on stem cells in the hair follicle to determine what switches them on. The researchers found cells produced by the stem cells, progeny known at Transit-Amplifying Cells or TACs, emit a signal that tells quiet hair follicle stem cells to become active.

"Many types of mammalian stem cells produce TACs, which act as an intermediate between the stem cells and their final product: fully differentiated cells in blood, skin and elsewhere," says Ya-Chieh Hsu, who conducted the research while as a postdoc in the lab and will soon move to Harvard University. "In the past, TACs were seen as a population of cells that sat by passively cranking out tissues. No one expected them to play a regulatory role."

Hsu and Fuchs went a step further to identify the signal sent out by the TACs. They pinpointed a cell-division promoting protein called Sonic Hedgehog, which plays a role in the embryonic development of the brain, eyes and limbs.

Stem cells are medically valuable because they have the potential to produce a number of specialized cells suitable for specific roles. Stem cells' production of these differentiated cells is crucial to normal maintenance, growth and repair. Many tissues have two populations of stem cells: one that divides rarely, known as the quiescent stem cells, and another that is more prone to proliferate, known as primed stem cells. Regardless of their proliferation frequency, most stem cells in humans do not directly produce differentiated progeny cells; instead, they give rise to an intermediate proliferating population, the TACs.

The hair follicle, the tiny organ that produces a hair, forms a narrow cavity down into the skin. It cycles between rounds of growth, destruction and rest. When entering the growth phase, the primed stem cell population is always the first to divide and generates the TACs clustered lower down in the hair follicle. Primed stem cell proliferation sets the stage for the next round of hair growth, a process which ensures hairs are replaced as they are lost over time. Proliferating TACs produce the hair shaft, as well as all the cells surrounding the hair underneath the skin, which make up the follicle itself.

At the outset, Hsu and Fuchs suspected a role for both the TACs and for Sonic Hedgehog in hair regeneration.

"We noticed that the primed stem cell population gets activated early and makes the TACs, while the quiescent stem cell population only becomes activated once TACs are generated. This correlation prompted us to look for a signal that is made by the TACs. Sonic Hedgehog is that signal, as we went on to demonstrate," explained Fuchs.

In experiments described this week in Cell, Hsu disabled TACs' ability to produce the Sonic Hedgehog protein by knocking out the gene responsible in the hair follicles of adult mice. As a result, the proliferation of hair follicle stem cells and their TACs are both compromised. They further showed that it is the quiescent stem cell population which requires Sonic Hedgehog directly for proliferation.

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Stem cell progeny tell their parents when to turn on

Beware of fake medicines and advertisements touting the purported miracles that stem cell therapy can do. This was the warning aired by former health secretary Esperanza Cabral at the Kapihan sa Manila at the Diamond Hotel last Monday.

Contrary to what the ads claim, she said, stem cell therapy has not been scientifically proven to cure any disease or make anyone young again. It has been successful in a very few experiments, which is the reason quack doctors are taking advantage of it to make exaggerated claims that the therapy can cure the deadliest diseases known to man.

The Food and Drug Administration (FDA) very recently issued a similar warning against it.

Stem cell therapy is the process of injecting into patients young cells taken from humans or sheep. The theory is that the young cells will rejuvenate the old cells of the patients and make them young again and cure whatever diseases they have. Although experiments are being conducted, no such results have been achieved. But that does not prevent foreign quack doctors from coming here and making all those exaggerated claims. Sadly, they are aided by some Filipino doctors.

The reason is that in countries like the Philippines where the people are suckers for miracle cures, stem cell therapyand other miracle curesis like a gold mine.

Aging millionaires looking for the fountain of youth pay a lot of money to undergo stem cell therapy. Patients with terminal illnesses like cancer, in a desperate search for a cure, also fall victim to the sales talk and word-of-mouth yarns of so-and-so being cured by the therapy.

But they get neither younger nor cured. And the quack doctors run laughing with their patients money all the way to the bank.

A friend told me that he had gone abroad to have stem cell therapy. He said he felt better and stronger after the treatment. Look at me, dont I look younger? he said.

I looked at him. He didnt look a minute younger and in fact looked the same as when I last saw him, maybe even older.

My wife said I look younger, he said. It was his wife who had convinced him to have the stem cell therapy.

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Dont be fooled by quacks and fake meds

PUBLIC RELEASE DATE:

9-May-2014

Contact: Nicole Giese Rura rura@wi.mit.edu 617-258-6851 Whitehead Institute for Biomedical Research

CAMBRIDGE, Mass. (May 9, 2014) Whitehead Institute scientists have identified a genetic cause of a facial disorder known as hemifacial microsomia (HFM). The researchers find that duplication of the gene OTX2 induces HFM, the second-most common facial anomaly after cleft lip and palate.

HFM affects approximately one in 3,500 births. While some cases appear to run in families, no gene had been found to be causative. That is until Whitehead Fellow Yaniv Erlich and his lab set out to do just that. Their work is described in this week's issue of the journal PLOS ONE.

Patients with HFM tend to have asymmetrical faces, --typically with one side of the upper and lower jaws smaller than the opposite side--a smaller or malformed ear on the affected side, and, in some cases, neurological or developmental abnormalities.

Thought to be brought on by circulation difficulties during embryonic development, HFM is also thought to be sporadicmeaning that it occurs spontaneously rather than through inheritance. However, one family in northern Israel has more than its share of the anomaly.

To identify the origin of this family's disorder, Erlich and lab technician Dina Zielinski began studying the genomes of a five-year-old female member of the family, along with those of her mother, grandmother, and male cousin, who all exhibited traits of HFM. Later, the genetic information from the grandmother's Russian cousin, who resides in the Philadelphia area, was recruited to the study.

"What's unique here is that this is the largest family with this disorder described in the literature," says Erlich. "Most of the time, you see one person affected, or perhaps two peoplea parent and a child. Such a large family increases the power of the genetic study and clearly signals that there is a genetic component to a disease."

To find the cause of this family's HFM, Zielinski began by searching for a point mutation, but the five of the study participants held no such mutation in common. Next she looked for sections of the genome that are duplicated. All had an extra copy of one 1.3 megabase pair section of chromosome 14. Duplications this large are frequently detrimental.

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Scientists find gene behind a highly prevalent facial anomaly

PUBLIC RELEASE DATE:

8-May-2014

Contact: Laura Kurtzman laura.kurtzman@ucsf.edu 415-502-6397 University of California - San Francisco

A scientific team led by the Gladstone Institutes and UC San Francisco has discovered that a common form of a gene already associated with long life also improves learning and memory, a finding that could have implications for treating age-related diseases like Alzheimer's.

The researchers found that people who carry a single copy of the KL-VS variant of the KLOTHO gene perform better on a wide variety of cognitive tests. When the researchers modeled the effects in mice, they found it strengthened the connections between neurons that make learning possible what is known as synaptic plasticity by increasing the action of a cell receptor critical to forming memories.

The discovery is a major step toward understanding how genes improve cognitive ability and could open a new route to treating diseases like Alzheimer's. Researchers have long suspected that some people may be protected from the disease because of their greater cognitive capacity, or reserve. Since elevated levels of the klotho protein appear to improve cognition throughout the lifespan, raising klotho levels could build cognitive reserve as a bulwark against the disease.

"As the world's population ages, cognitive frailty is our biggest biomedical challenge," said Dena Dubal, MD, PhD, assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at UCSF and lead author of the study, published May 8 in Cell Reports. "If we can understand how to enhance brain function, it would have a huge impact on people's lives."

Klotho was discovered in 1997 and named after the Fate from Greek mythology who spins the thread of life. The investigators found that people who carry a single copy of the KL-VS variant of the KLOTHO gene, roughly 20 percent of the population, have more klotho protein in their blood than non-carriers. Besides increasing the secretion of klotho, the KL-VS variant may also change the action of the protein and is known to lessen age-related cardiovascular disease and promote longevity.

The team's report is the first to link the KL-VS variant, or allele, to better cognition in humans, and buttresses these findings with genetic, electrophysiological, biochemical and behavioral experiments in mice. The researchers tested the associations between the allele and age-related human cognition in three separate studies involving more than 700 people without dementia between the ages of 52 and 85. Altogether, it took about three years to conduct the work.

"These surprising results pave a promising new avenue of research," said Roderick Corriveau, Ph.D., program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS). "Although preliminary, they suggest klotho could be used to bump up cognition for people suffering from dementia."

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Better cognition seen with gene variant carried by 1 in 5

PUBLIC RELEASE DATE:

9-May-2014

Contact: Christopher G. Thomas thomaschr@ninds.nih.gov 301-496-5751 NIH/National Institute of Neurological Disorders and Stroke

Scientists showed that people who have a variant of a longevity gene, called KLOTHO, have improved brain skills such as thinking, learning and memory regardless of their age, sex, or whether they have a genetic risk factor for Alzheimer's disease. Increasing KLOTHO gene levels in mice made them smarter, possibly by increasing the strength of connections between nerve cells in the brain. The study was partly funded by the National Institutes of Health.

"This could be a major step toward helping millions around the world who are suffering from Alzheimer's disease and other dementias," said Dena Dubal, M.D., Ph.D., an assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at the University of California San Francisco (UCSF) and the lead author of the study published in Cell Reports. "If we could boost the brain's ability to function, we may be able to counter dementias."

As people live longer the effects of aging on the brain will become a greater health issue. This is especially true for dementias, a collection of brain disorders that can cause memory problems, impaired language skills and other symptoms. With the number of dementia cases worldwide estimated to double every 20 years from 35.6 million people in 2010 to 65.7 million in 2030 and 115.4 million in 2050, the need for treatments is growing.

Klotho is the name of a Greek mythological goddess of fate, "who spins the thread of life." People who have one copy of a variant, or form, of the KLOTHO gene, called KL-VS, tend to live longer and have lower chances of suffering a stroke whereas people who have two copies may live shorter lives and have a higher risk of stroke. In this study, the investigators found that people who had one copy of the KL-VS variant performed better on a battery of cognitive tests than subjects who did not have it, regardless of age, sex or the presence of the apolipoprotein 4 gene, the main genetic risk factor for Alzheimer's disease.

"This study shows the importance of genes that regulate the multiple aging processes involved in the maintenance of cognitive function," said Suzana Petanceska, Ph.D., program director in NIA's Division of Neuroscience. "Understanding the factors that control the levels and activity of KLOTHO across multiple organ systems may open new therapeutic avenues for prevention of age-related cognitive decline and dementia."

The investigators tested a variety of cognitive skills, including learning, memory, and attention. More than 700 subjects, 52 to 85 years old were tested as part of three studies. None had any sign of dementia. Consistent with previous studies, 20 to 25 percent of the subjects had one copy of the KL-VS variant and performed better on the tests than those who had no copies. Performance on the tests decreased with age regardless of whether a subject had one or no copies of the KL-VS gene variant.

The KLOTHO gene provides the blueprint for a protein made primarily by the cells of the kidney, placenta, small intestine, and prostate. A shortened version of the protein can circulate through the blood system. Blood tests showed that subjects who had one copy of the KL-VS variant also had higher levels of circulating klotho protein. The levels decreased with age as others have observed. The researchers speculate that the age-related decrease in circulating levels of klotho protein may have caused some of the decline in performance on the cognitive tests.

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Longevity gene may boost brain power

SAY NO TO GENETIC ENGINEERING ! SWINE FLU 2009

By: Tarian Tradisional

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SAY NO TO GENETIC ENGINEERING ! SWINE FLU 2009 - Video

Genetic Engineering Intro
Video Scribe Project.

By: Kim Diot

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Genetic Engineering Intro - Video

Genetic Engineering Simplified
Our team made a brief explanation about Genetic Engineering. Don #39;t forget to visit http://www.chemistriology.webs.com for more videos.

By: Chemistriology

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Genetic Engineering Simplified - Video