ScienceDaily (May 14, 2012) — A team of international scientists has made a significant breakthrough in understanding the cause of bile duct cancer, a deadly type of liver cancer. By identifying several new genes frequently mutated in bile duct cancers, researchers are paving the way for better understanding of how bile duct cancers develop.

Their discovery is published online in Nature Genetics.

Bile Duct Cancer, or Cholangiocarcinoma, is a fatal cancer with a poor prognosis. Accounting for 10 to 25 per cent of all primary liver cancers worldwide, bile duct cancer is a prevalent disease in Southeast Asia, particularly in Northeast Thailand, which sees about 20,000 new cases each year. The high incidence in Thailand is attributed to long-term consumption of raw fish infected with liver flukes — food-borne parasites found in fish. Liver fluke infections are widespread in Northeast Thailand, where they are thought to occur in over 6 million people. Once eaten, the flukes accumulate in the bile ducts of the human host, causing constant infection and eventually the onset of cancer.

The research team was led by Bin Tean Teh, M.D., Ph.D., Director and Principal Investigator of the NCCS-VARI Translational Cancer Research Laboratory. Van Andel Research Institute (VARI) and the National Cancer Center, Singapore (NCCS) established the NCCS-VARI Translational Research Program at the National Cancer Center, Singapore in 2007. The program focuses on the biology behind varying drug responses in Asian versus non-Asian patients with specific types of cancer.

The team also included Associate Professor Patrick Tan, Associate Professor Steve Rozen (both of Duke-NUS Graduate Medical School of Singapore) and Professor Vajarabhongsa Bhudhisawasdi from Thailand’s Khon Kaen University. The breakthrough came after two years of intensive research, which saw scientists from Singapore visiting the villagers in northern Thailand, and Thai researchers coming to Singapore to work in NCCS laboratories.

Professor Teh said the study will pave the way for a better understanding of the roles that newly identified genes play in the development of bile duct cancer.

“This discovery adds depth to what we currently know about bile duct cancer,” said Teh. “More important is that we are now aware of new genes and their effects on bile duct cancer, and we now need to further examine their biological aspects to determine how they bring about the onset of Cholangiocarcinoma.”

Using state of the art DNA sequencing, the researchers analysed eight bile duct cancers and normal tissues from Thai patients, and discovered mutations in 187 genes. The team then selected 15 genes that were frequently mutated for further analysis in an additional 46 cases. Many of these genes, such as MLL3, ROBO2 and GNAS, have not been previously implicated in bile duct cancers.

“With this finding we now know much more about the molecular mechanisms of the disease and we can draw up additional measures that can be taken while we identify the most appropriate treatment protocols. We are talking about the potential to save many lives in Thailand,” said Professor Vajarabhongsa Bhudhisawasdi, Director of the Liver Fluke and Cholangiocarcinoma Research Center, Khon Kaen University of Thailand. “Also, this study shows that we can work closely with our counterparts in other countries and share our expertise and experience to improve the lot for the people.”

The researchers also compared the bile duct cancers to other related cancers of the liver and pancreas. Surprisingly, they found that the bile ducts cancers shared certain similarities with pancreatic cancer.

“This research provides a strong direction for future studies,” said Associate Professor Patrick Tan, faculty member of the Cancer and Stem Cell Biology Programme at the Duke-NUS. “Cholangiocarcinoma and Pancreatic Duct Adenocarcinoma appear to share more molecular similarities than earlier studies had indicated, and suggest that there are common biological pathways between the two cancers. By studying these pathways, we can then shed more light on how these tumours develop.”

Dr. Chutima Subimerb, a Thai scientist involved in the project, said she was pleased with the collaboration and to be able to participate in this health diplomacy project. “We are very privileged to be able to work alongside Prof Teh and the other scientists from Singapore. By pooling our resources we were able to make this discovery which will have very wide impact on the people, especially the poor people who have been eating the fish that they catch from the ponds and rivers in the region. I believe this is only a first step and we will see even more collaborations in time to come between our two countries in the field of scientific research.”

The research was funded by the Singapore Ministry of Health’s National Medical Research Council, Millennium Foundation, Lee Foundation, National Cancer Centre Research Fund, Duke-NUS Graduate Medical School Singapore, Cancer Science Institute Singapore, Research Team Strengthening Grant, National Genetic Engineering and Biotechnology Center and the National Science and Technology Development Agency (Thailand).

Journal Reference:

1. Choon Kiat Ong, Chutima Subimerb, Chawalit Pairojkul, Sopit Wongkham, Ioana Cutcutache, Willie Yu, John R McPherson, George E Allen, Cedric Chuan Young Ng, Bernice Huimin Wong, Swe Swe Myint, Vikneswari Rajasegaran, Hong Lee Heng, Anna Gan, Zhi Jiang Zang, Yingting Wu, Jeanie Wu, Ming Hui Lee, DaChuan Huang, Pauline Ong, Waraporn Chan-on, Yun Cao, Chao-Nan Qian, Kiat Hon Lim, Aikseng Ooi, Karl Dykema, Kyle Furge, Veerapol Kukongviriyapan, Banchob Sripa, Chaisiri Wongkham, Puangrat Yongvanit, P Andrew Futreal, Vajarabhongsa Bhudhisawasdi, Steve Rozen, Patrick Tan, Bin Tean Teh. Exome sequencing of liver fluke–associated cholangiocarcinoma. Nature Genetics, 2012; DOI: 10.1038/ng.2273

ScienceDaily (May 15, 2012) — Researchers at the University of California, San Diego School of Medicine and Moores Cancer Center have identified a new biomarker and therapeutic target for pancreatic cancer, an often-fatal disease for which there is currently no reliable method for early detection or therapeutic intervention.

The paper will be published May 15 in Cancer Research.

Pancreatic ductal adenocarcinoma, or PDAC, is the fourth-leading cause of cancer-related death. Newly diagnosed patients have a median survival of less than one year, and a 5-year survival rate of only 3 to 5 percent. Therefore, biomarkers that can identify early onset of PDAC and which could be viable drug targets are desperately needed.

‘”We found that a kinase called PEAK1 is turned on very early in pancreatic cancer,” said first author Jonathan Kelber, PhD, a postdoctoral researcher in the UCSD Department of Pathology and Moores Cancer Center. “This protein was clearly detected in biopsies of malignant tumors from human patients — at the gene and the protein levels — as well as in mouse models.”

PEAK1 is a type of tyrosine kinase — an enzyme, or type of protein, that speeds up chemical reactions and acts as an “on” or “off” switch in many cellular functions. The fact that PEAK1 expression is increased in human PDAC and that its catalytic activity is important for PDAC cell proliferation makes it an important candidate as a biomarker and therapeutic target for small molecule drug discovery.

In addition to showing that levels of PEAK1 are increased during PDAC progression, the scientists found that PEAK1 is necessary for the cancer to grow and metastasize.

“PEAK1 is a critical signaling hub, regulating cell migration and proliferation,” said Kelber. “We found that if you knock it out in PDAC cells, they form significantly smaller tumors in preclinical mouse models and fail to metastasize efficiently.”

The research team, led by principal investigator Richard Klemke, PhD, UCSD professor of pathology, studied a large, on-line data base of gene expression profiles to uncover the presence of PEAK1 in PDAC. These findings were corroborated at the protein level in patient biopsy samples from co-investigator Michael Bouvet, MD, and in mouse models developed by Andrew M. Lowy, MD, both of the UCSD Department of Surgery at Moores Cancer Center.

While many proteins are upregulated in cancers of the pancreas, there has been limited success in identifying candidates that, when inhibited, have potential as clinically approved therapeutics. However, the researchers found that inhibition of PEAK1-dependent signaling sensitized PDAC cells to existing chemotherapies such as Gemitabine, and immunotherapies such as Trastuzumab.

“Survival rates for patients with pancreatic cancer remain low,” said Bouvet. “Therefore, earlier detection and novel treatment strategies are very important if we are going to make any progress against pancreatic cancer. Since current therapies are often ineffective, our hope is that the findings from this research will open up a new line of investigation to bring a PEAK1 inhibitor to the clinic.”

Additional contributors to the study include Theresa Reno, Sharmeela Kaushal, Cristina Metildi,Tracy Wright, Konstantin Stoletov, Jessica M. Weems, Frederick D. Park, Evangeline Mose, UC San Diego; Yingchun Wang, Chinese Academy of Science, Beijing; and Robert M. Hoffman, UC San Diego and AntiCancer, Inc., San Diego.

The study was supported by the National Institutes of Health.

Journal Reference:

1. J. A. Kelber, T. Reno, S. Kaushal, C. Metildi, T. Wright, K. Stoletov, J. M. Weems, F. D. Park, E. Mose, Y. Wang, R. M. Hoffman, A. M. Lowy, M. Bouvet, R. L. Klemke. KRas Induces a Src/PEAK1/ErbB2 Kinase Amplification Loop That Drives Metastatic Growth and Therapy Resistance in Pancreatic Cancer. Cancer Research, 2012; 72 (10): 2554 DOI: 10.1158/0008-5472.CAN-11-3552

ScienceDaily (May 15, 2012) — A drug made from the saliva of the Gila monster lizard is effective in reducing the craving for food. Researchers at the Sahlgrenska Academy, University of Gothenburg, have tested the drug on rats, who after treatment ceased their cravings for ordinary food and also chocolate.An increasing number of patients suffering from type 2 diabetes are offered a pharmaceutical preparation called Exenatide, which helps them to control their blood sugar. The drug is a synthetic version of a natural substance called exendin-4, which is obtained from a rather unusual source — the saliva of the Gila monster lizard (Heloderma suspectum), North America’s largest lizard.

Unexpected effect

Researchers at the Sahlgrenska Academy at the University of Gothenburg, have now found an entirely new and unexpected effect of the lizard substance.

Reduces cravings for food

In a study with rats published in the Journal of Neuroscience,Assistant Professor Karolina Skibicka and her colleagues show that exendin-4 effectively reduces the cravings for food.

“This is both unknown and quite unexpected effect,” comments an enthusiastic Karolina Skibicka: “Our decision to eat is linked to the same mechanisms in the brain which control addictive behaviours. We have shown that exendin-4 affects the reward and motivation regions of the brain.”

Significant findings

The implications of the findings are significant” states Suzanne Dickson, Professor of Physiology at the Sahlgrenska Academy: “Most dieting fails because we are obsessed with the desire to eat, especially tempting foods like sweets. As exendin-4 suppresses the cravings for food, it can help obese people to take control of their weight,” suggests Professor Dickson.

Treatment for eating disorders

Research on exendin-4 also gives hope for new ways to treat diseases related to eating disorders, for example, compulsive overeating.

Another hypothesis for the Gothenburg researchers’ continuing studies is that exendin-4 may be used to reduce the craving for alcohol.

“It is the same brain regions which are involved in food cravings and alcohol cravings, so it would be very interesting to test whether exendin-4 also reduces the cravings for alcohol,” suggests Assistant Professor Skibicka.

Journal Reference:

1. Suzanne L. Dickson, Rozita H. Shirazi, Caroline Hansson, Filip Bergquist, Hans Nissbrandt, and Karolina P. Skibicka.The Glucagon-Like Peptide 1 (GLP-1) Analogue, Exendin-4 Decreases the Rewarding Value of Food: A New Role for the Mesolimbic GLP-1 Receptors. Journal of Neuroscience, April 4, 2012 DOI:10.1523/%u200BJNEUROSCI.6326-11.2012

Dr. Weeks’ Comment:  Baclofen is an old medication which is a muscle relaxant. Typically it was used to lessen the muscle spasms of cerebral palsy or multiple sclerosis.  Years ago, we starting recommending it for alcoholism after the courageous book  “The End of My Addiction”  written by a French surgeon.  Now we find, like Oxytocin,  Baclofen can help with the symptoms of autism.  Given its low side-effect profile, this merits closer study.

Addiction Drug for Autism Patients

History of Baclofen

Baclofen was originally used in the 1920s to help with cerebral palsy. It is a muscle relaxer and antispastic agent. It has a way of calming muscles, relieving pain, and decreasing stiffness in patients with cerebral palsy, multiple sclerosis, and epilepsy. Baclofen works on a neurotransmitter in the brain called GABA, which makes it also effective for the treatment of addiction. Baclofen increases GABA activity, which is the same effect alcohol and some drugs have on the brain. The result is a calming of the brain, and a decrease in anxiety. Doctors have been using baclofen to treat people with drug addiction and alcoholism since the 1980s.

Baclofen for Autism

This is the same effect researchers are hoping the new form of this drug will have on a different group of people. Children with autism have been found to benefit from a reformulated version of baclofen, called STX209. Researchers are studying this drug and its effects on autistic children and have found a reduction in behavioral outbursts and an increase in social behavior and communication. The children become more relaxed, more comfortable, and not as anxious as they normally would be.

Benefit for Addiction Treatment

The development of STX209 and its treatment for autistic patients may also benefit the field of addiction treatment. It could be that this medication has more potential than was originally thought. We know it can help with addiction, because it helps reduce anxiety in these patients. With the trials for autism treatment, researchers have separated out baclofen into two components, and begun using the active part of this drug, called STX209. This new drug is more potent than baclofen and may more effectively treat addiction patients also.

There is much research to be done on this drug before it is given the go ahead to use. Scientists are learning much along the way about how a drug addict or alcoholic can be similar to an autistic child. These two conditions, while such different diseases, seem to have somewhat of a connection. Maybe it has to do with how the brain handles stress, or the effects of anxiety on the mind. But hopefully with more studies, we will have a better treatment someday for autism. Someone that suffers from addiction may also be able to benefit from a medication like this during treatment, but there is no quick fix for conditions like addiction. Any medication given will need to be followed up with treatment and therapy in order to help the recovering addict stay sober without the aid of medication.

Sources

Revamped Meds May Help With Autism & Special Needs

New Version of an Old Drug Could Treat Autism (and Addiction Too)

Baclofen

Heart Surgeon Speaks Out On What Really Causes Heart Disease

These recommendations are no longer scientifically or morally defensible. The discovery a few years ago that inflammation in the artery wall is the real cause of heart disease is slowly leading to a paradigm shift in how heart disease and other chronic ailments will be treated.

The long-established dietary recommendations have created epidemics of obesity and diabetes, the consequences of which dwarf any historical plague in terms of mortality, human suffering and dire economic consequences.

Despite the fact that 25% of the population takes expensive statin medications and despite the fact we have reduced the fat content of our diets, more Americans will die this year of heart disease than ever before. 

Statistics from the American Heart Association show that 75 million Americans currently suffer from heart disease, 20 million have diabetes and 57 million have pre-diabetes. These disorders are affecting younger and younger people in greater numbers every year.

Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped.

Inflammation is not complicated — it is quite simply your body’s natural defence to a foreign invader such as a bacteria, toxin or virus. The cycle of inflammation is perfect in how it protects your body from these bacterial and viral invaders. However, if we chronically expose the body to injury by toxins or foods the human body was never designed to process,a condition occurs called chronic inflammation. Chronic inflammation is just as harmful as acute inflammation is beneficial.

What thoughtful person would willfully expose himself repeatedly to foods or other substances that are known to cause injury to the body? Well, smokers perhaps, but at least they made that choice willfully.

The rest of us have simply followed the recommended mainstream diet that is low in fat and high in polyunsaturated fats and carbohydrates, not knowing we were causing repeated injury to our blood vessels. This repeated injury creates chronic inflammation leading to heart disease, stroke, diabetes and obesity.

Let me repeat that: The injury and inflammation in our blood vessels is caused by the low fat diet recommended for years by mainstream medicine. 

What are the biggest culprits of chronic inflammation? Quite simply, they are the overload of simple, highly processed carbohydrates (sugar, flour and all the products made from them) and the excess consumption of omega-6 vegetable oils like soybean, corn and sunflower that are found in many processed foods. 

Take a moment to visualize rubbing a stiff brush repeatedly over soft skin until it becomes quite red and nearly bleeding. you kept this up several times a day, every day for five years. If you could tolerate this painful brushing, you would have a bleeding, swollen infected area that became worse with each repeated injury. This is a good way to visualize the inflammatory process that could be going on in your body right now.

Regardless of where the inflammatory process occurs, externally or internally, it is the same. I have peered inside thousands upon thousands of arteries. A diseased artery looks as if someone took a brush and scrubbed repeatedly against its wall. Several times a day, every day, the foods we eat create small injuries compounding into more injuries, causing the body to respond continuously and appropriately with inflammation.

While we savor the tantalizing taste of a sweet roll, our bodies respond alarmingly as if a foreign invader arrived declaring war. Foods loaded with sugars and simple carbohydrates, or processed with omega-6 oils for long shelf life have been the mainstay of the American diet for six decades. These foods have been slowly poisoning everyone.

How does eating a simple sweet roll create a cascade of inflammation to make you sick?

Imagine spilling syrup on your keyboard and you have a visual of what occurs inside the cell. When we consume simple carbohydrates such as sugar, blood sugar rises rapidly. In response, your pancreas secretes insulin whose primary purpose is to drive sugar into each cell where it is stored for energy. If the cell is full and does not need glucose, it is rejected to avoid extra sugar gumming up the works.

When your full cells reject the extra glucose, blood sugar rises producing more insulin and the glucose converts to stored fat.

What does all this have to do with inflammation? Blood sugar is controlled in a very narrow range. Extra sugar molecules attach to a variety of proteins that in turn injure the blood vessel wall. This repeated injury to the blood vessel wall sets off inflammation. When you spike your blood sugar level several times a day, every day, it is exactly like taking sandpaper to the inside of your delicate blood vessels. 

While you may not be able to see it, rest assured it is there. I saw it in over 5,000 surgical patients spanning 25 years who all shared one common denominator — inflammation in their arteries.

Let’s get back to the sweet roll. That innocent looking goody not only contains sugars, it is baked in one of many omega-6 oils such as soybean. Chips and fries are soaked in soybean oil; processed foods are manufactured with omega-6 oils for longer shelf life. While omega-6′s are essential -they are part of every cell membrane controlling what goes in and out of the cell — they must be in the correct balance with omega-3′s.

If the balance shifts by consuming excessive omega-6, the cell membrane produces chemicals called cytokines that directly cause inflammation.

Today’s mainstream American diet has produced an extreme imbalance of these two fats. The ratio of imbalance ranges from 15:1 to as high as 30:1 in favor of omega-6. That’s a tremendous amount of cytokines causing inflammation. In today’s food environment, a 3:1 ratio would be optimal and healthy. 

To make matters worse, the excess weight you are carrying from eating these foods creates overloaded fat cells that pour out large quantities of pro-inflammatory chemicals that add to the injury caused by having high blood sugar. The process that began with a sweet roll turns into a vicious cycle over time that creates heart disease, high blood pressure, diabetes and finally, Alzheimer’s disease, as the inflammatory process continues unabated.

There is no escaping the fact that the more we consume prepared and processed foods, the more we trip the inflammation switch little by little each day. The human body cannot process, nor was it designed to consume, foods packed with sugars and soaked in omega-6 oils.

There is but one answer to quieting inflammation, and that is returning to foods closer to their natural state. To build muscle, eat more protein. Choose carbohydrates that are very complex such as colorful fruits and vegetables. Cut down on or eliminate inflammation- causing omega-6 fats like corn and soybean oil and the processed foods that are made from them.

One tablespoon of corn oil contains 7,280 mg of omega-6; soybean contains 6,940 mg. Instead, use olive oil or butter from grass-fed beef.

Animal fats contain less than 20% omega-6 and are much less likely to cause inflammation than the supposedly healthy oils labelled polyunsaturated. Forget the “science” that has been drummed into your head for decades. The science that saturated fat alone causes heart disease is non-existent. The science that saturated fat raises blood cholesterol is also very weak. Since we now know that cholesterol is not the cause of heart disease, the concern about saturated fat is even more absurd today.

The cholesterol theory led to the no-fat, low-fat recommendations that in turn created the very foods now causing an epidemic of inflammation. Mainstream medicine made a terrible mistake when it advised people to avoid saturated fat in favor of foods high in omega-6 fats. We now have an epidemic of arterial inflammation leading to heart disease and other silent killers.

What you can do is choose whole foods your grandmother served and not those your mom turned to as grocery store aisles filled with manufactured foods. By eliminating inflammatory foods and adding essential nutrients from fresh unprocessed food, you will reverse years of damage in your arteries and throughout your body from consuming the typical American diet.

To increase the genetic diversity of U.S. corn, the Germplasm Enhancement for Maize project seeks to combine exotic germplasm, such as this unusually shaped maize from Latin America with domestic corn

The Polish position on GMO is sceptical. According to the government’s policy, Poland intends to be a GMO-free country – it was stipulated in the government’s position on GMO in 2008.

At the moment, the EU law does not provide a possibility to say a decisive

“NO to GMO”, but it allows using so-called exemptions, if human and animal health

or life or natural environment is at risk – the Polish Ministry of Agriculture is currently taking advantage of this possibility. As far as maize is concerned, the ministry will introduce a regulation forbidding cultivation of genetically modified maize throughout Poland (MON 810 maize) – the draft version of March 15th has been sent to the public consultation.

The ban is justified by the threat of pollution of areas where bees collect nectar with genetically modified pollen and the resulting damage to Polish bee-keepers. As far as the ban on cultivation of genetically modified potato (Amflora) is concerned, currently there is no evidence proving its harmfulness, so the exemption cannot be applied. It should, however, be pointed out that there is no information that Polish farmers are interested in its cultivation.

These are not the only actions taken by the government. At the beginning of April, the Ministry of Environment prepared and sent to the public consultation the draft act on genetically modified organisms. The draft concerns technical issues related to the closed use of GMM and GMO, i.e. handling genetically modified micro-organisms and organisms in closed systems, e.g. in laboratories, greenhouses, etc., mainly during scientific research. The scope included in the new draft will be sufficient to ensure that once Poland adopts these regulations it will have legal norms compliant with EU law with respect to GMM (genetically modified micro-organisms). The act will be particularly important to scientists. Among other things, a simplification of procedures for obtaining permits for conducting work in laboratories is planned. The act will guarantee a high level of safety for research. Thanks to the modern act, it will be possible in Poland to safely conduct research important for the development of medicine (clinical research in which GMM and GMO are used) and pharmacology (manufacturing of, for example, medicines and vaccines).

The GMO regulations which are currently applicable in Poland do not regulate all issues connected with it which are regulated by the EU law, e.g. the manner in which cultivations of genetically modified plants are to be conducted and registered or supervision of such cultivations. The GMO issue in Poland requires new regulations, for example due to the need to adjust the law to the current EU regulations and the need to follow the fast technological progress in this field.

The discussion on the future of GMO has been underway in the Council for nearly 10 years. During the debate, the Member States have demanded the right to more independent actions with respect to the issue of making decisions about GMO crops in their territory. At meetings of the so-called GMO ad hoc group, which Poland was in charge of in the second half of 2011, we called for agreement and resumption of the work on EU decisions, but the differences in positions of the Member States are still very significant, also during the current Danish presidency. The aim of the group’s work was to obtain Council’s consent for adopting a new legal act which would enable the Member States to introduce bans on GMO crops in their territory.

Once it is possible to coordinate the national and EU processes, an additional (for draft versions of the Ministry Environment and Ministry of Agriculture) “big” act on GMO will be prepared in Poland, which will regulate, among other things, the issue of exemption of the country from GMO crops.

Source: the Chancellery of the Prime Minister

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10.World Health Organization. Environmental Health Criteria 118: Inorganic Mercury. Geneva: World Health Organization, 1992.

ScienceDaily (May 11, 2012) — Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven, succeeded in undoing the effect of one of the genetic defects that leads to Parkinson’s using vitamin K2. His discovery gives hope to Parkinson’s patients.

This research was done in collaboration with colleagues from Northern Illinois University (US) and was recently published in the journalScience.

“It appears from our research that administering vitamin K2 could possibly help patients with Parkinson’s. However, more work needs to be done to understand this better,” says Patrik Verstreken.

Malfunctioning power plants are at the basis of Parkinson’s.

If we looked at cells as small factories, then mitochondria would be the power plants responsible for supplying the energy for their operation. They generate this energy by transporting electrons. In Parkinson’s patients, the activity of mitochondria and the transport of electrons have been disrupted, resulting in the mitochondria no longer producing sufficient energy for the cell. This has major consequences as the cells in certain parts of the brain will start dying off, disrupting communication between neurons. The results are the typical symptoms of Parkinson’s: lack of movement (akinesia), tremors and muscle stiffness.

The exact cause of this neurodegenerative disease is not known. In recent years, however, scientists have been able to describe several genetic defects (mutations) found in Parkinson’s patients, including the so-called PINK1 and Parkin mutations, which both lead to reduced mitochondrial activity. By studying these mutations, scientists hope to unravel the mechanisms underlying the disease process.

Paralyzed fruit flies

Fruit flies (Drosophila) are frequently used in lab experiments because of their short life spans and breeding cycles, among other things. Within two weeks of her emergence, every female is able to produce hundreds of offspring. By genetically modifying fruitflies, scientists can study the function of certain genes and proteins. Patrik Verstreken and his team used fruitflies with a genetic defect in PINK1 or Parkin that is similar to the one associated with Parkinson’s. They found that the flies with a PINK1 or Parkin mutation lost their ability to fly.

Upon closer examination, they discovered that the mitochondria in these flies were defective, just as in Parkinson’s patients. Because of this they generated less intracellular energy — energy the insects needed to fly. When the flies were given vitamin K2, the energy production in their mitochondria was restored and the insects’ ability to fly improved. The researchers were also able to determine that the energy production was restored because the vitamin K2 had improved electron transport in the mitochondria. This in turn led to improved energy production.

Conclusion

Vitamin K2 plays a role in the energy production of defective mitochondria. Because defective mitochondria are also found in Parkinson’s patients with a PINK1 or Parkin mutation, vitamin K2 potentially offers hope for a new treatment for Parkinson’s.Journal Reference:

1. M. Vos, G. Esposito, J. N. Edirisinghe, S. Vilain, D. M. Haddad, J. R. Slabbaert, S. Van Meensel, O. Schaap, B. De Strooper, R. Meganathan, V. A. Morais, P. Verstreken.Vitamin K2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency. Science, 2012; DOI:10.1126/science.1218632