Protein Treatment Staves Off Alzheimer’s Disease Symptoms

Protein Treats Alzheimer’s Disease

Protein Treats Alzheimer’s Disease

Alzheimer’s disease is the sixth leading cause of death in the United States, with over 1,200 individuals developing the disease every day. A new paper in the Journal of Neuroscience from lead author Dena Dubal of the University of California, San Francisco describes how manipulating levels of a protein associated with memory can stave off Alzheimer’s symptoms, even in the presence of the disease-causing toxins.

Klotho is a transmembrane protein associated with longevity. The body makes less of this protein over time, and low levels of klotho is connected to a number of diseases including osteoporosis, heart disease, increased risk of stroke, and decreased cognitive function. These factors lead to diminished quality of life and even early death.

Previous research has shown that increasing klotho levels in healthy mice leads to increased cognitive function. This current paper from Dubal’s team builds on that research by increasing klotho in mice who are also expressing large amounts of amyloid-beta and tau, proteins that are associated with the onset of Alzheimer’s disease. Remarkably, even with high levels of these toxic, disease-causing proteins, the mice with elevated klotho levels were able to retain their cognitive function.

“It’s remarkable that we can improve cognition in a diseased brain despite the fact that it’s riddled with toxins,” Dubal said in a press release. “In addition to making healthy mice smarter, we can make the brain resistant to Alzheimer-related toxicity. Without having to target the complex disease itself, we can provide greater resilience and boost brain functions.”

The mechanism behind this cognitive preservation appears to be klotho interacting with a glutamate receptor called NMDA, which is critically important to synaptic transmission, thus influencing learning, memory, and executive function. Alzheimer’s disease typically damages these receptors, but the mice with elevated klotho were able to retain both NMDA function and cognition. Part of the success also appears to be due to the preservation of the NMDA subunit GluN2B, which existed in significantly larger numbers than the control mice. The mechanism and the results of this study will need to be investigated further before developing it into a possible treatment for humans in the future.

“The next step will be to identify and test drugs that can elevate klotho or mimic its effects on the brain,” added senior author Lennart Mucke from Gladstone Institutes. “We are encouraged in this regard by the strong similarities we found between klotho’s effects in humans and mice in our earlier study. We think this provides good support for pursuing klotho as a potential drug target to treat cognitive disorders in humans, including Alzheimer’s disease.”

 

Source:  iflscience.com

Scientists create organism with ‘Alien’ DNA

organism with 'alien' DNA

organism with ‘alien’ DNA

Scientists have created the first “semi-synthetic” micro-organism with a radically different genetic code from the rest of life on Earth.

The researchers believe the breakthrough is the first step towards creating new microbial life-forms with novel industrial or medical properties resulting from a potentially massive expansion of genetic information.

The semi-synthetic microbe, a genetically modified E. coli bacterium, has been endowed with an extra artificial piece of DNA with an expanded genetic alphabet – instead of the usual four “letters” of the alphabet its DNA molecule has six.

The natural genetic code of all living things is based on a sequence of four bases – G, C, T, A – which form two sets of bonded pairs, G to C and T to A, that link the two strands of the DNA double helix.

The DNA of the new semi-synthetic microbe, however, has a pair of extra base pairs, denoted by X and Y, which pair up together like the other base pairs and are fully integrated into the rest of the DNA’s genetic code.

The scientists said that the semi-synthetic E. coli bacterium replicates normally and is able to pass on the new genetic information to subsequent generations. However, it was not able to use the new encoded information to produce any novel proteins – the synthetic DNA was added as an extra circular strand that did not take part in the bacterium’s normal metabolic functions.

The study, published in the journal Nature, is the first time that scientists have managed to produce a genetically modified microbe that is able to function and replicate with a different genetic code to the one that is thought to have existed ever since life first started to evolve on Earth more than 3.5 billion years ago.

“Life on earth in all its diversity is encoded by only two pairs of DNA bases, A-T and C-G, and what we’ve made is an organism that stably contains those two plus a third, unnatural pair of bases,” said Professor Floyd Romesberg of the Scripps Research Institute in La Jolla, California.

“This shows that other solutions to storing information are possible and, of course, takes us closer to an expanded-DNA biology that will have many exciting applications, from new medicines to new kinds of nanotechnology,” Professor Romesberg said.

Expanding the genetic code with an extra base pair raises the prospect of building new kinds of proteins from a much wider range of amino acids than the 20 or so that exist in nature. A new code based on six base pairs could in theory deal with more than 200 amino acids, the scientists said.

“In principle, we could encode new proteins made from new, unnatural amino acids, which would give us greater power than ever to tailor protein therapeutics and diagnostics and laboratory reagents to have desired functions,” Professor Romesberg said.

“Other applications, such as nanomaterials, are also possible,” he added.

The researchers emphasised that there is little danger of the new life-forms living outside the confines of the laboratory, as they are not able to replicate with their synthetic DNA strand unless they are continuously fed the X and Y bases – synthetic chemicals called “d5SICS” and “dNaM”, that do not exist in nature.

The bacteria also need a special protein to transport the new bases around the cell of the microbe. The transporter protein comes from algae and if it, or the X and Y bases, are lacking, the microbial cells revert back to the natural genetic code, said Denis Malyshev of the Scripps Institute.

“Our new bases can only get into the cell if we turn on the “base transporter” protein. Without this transporter or when the new bases are not provided, the cell will revert back to A, T, G, C and the d5SICS and the dNaM will disappear from the genome,” Dr Malyshev said.

 

Source:  independent.co.uk

Gluten Causes Weight Gain

The case against gluten seems to have been closed with recent research from a Brazilian research team that published a report in the January 2013 Journal of Nutritional Biochemistry. It seems to have put an exclamation point on the wheat belly controversy.

The Study


Lacking scientific data confirming the mechanics of how gluten may or may not affect obesity, the study was set up to examine the differences in specific genetic and biochemical markers between rats fed gluten and rats that were kept gluten free.

The “wheat belly” syndrome and how it leads to other health issues was the purpose of their research. The research team chose biological markers that could indicate the onset of obesity and metabolic syndrome, precursors to diabetes and cardiac issues.

Both groups of rats were fed high fat diets. But one group was gluten free and the other group’s diet was 4.5 percent gluten. Even without tracing their predetermined markers, it was obvious the gluten free mice exhibited weight loss without any trace of lipid (fat) excretion.

An Analysis Of The Study


Sayer Ji of GreenmedInfo.com proposed this analysis: “… the weight gain associated with wheat consumption has little to do with caloric content per se; rather, the gluten proteins … disrupt endocrine and exocrine processes within the body, as well as directly modulating nuclear gene expression … to alter mamalian metabolism in the direction of weight gain.”

This study report, according to Sayer Ji proves that the major factor of obesity is gluten, not calories. Considering that both groups of mice were fed high fat diets and the gluten free mice lost weight without excreting lipids also implies that fat free diets for losing weight are bogus. This has been suspected by other nutritional experts who’ve abandoned matrix thinking.

Sayer Ji recommends that those who are overweight, pre-diabetic, experiencing metabolic syndrome, or suffering from irritable bowel syndrome try avoiding gluten grains, especially wheat, to determine from experience if gluten is the underlying cause.

There is evidence that gluten can be a factor in gut and psychology syndrome (GAPS) and even autism. (http://www.naturalnews.com/033094_gut_health_brain.html)

So How Did Wheat, “The Staff of Life,” Become A Weed of Disease?


Wheat is not the same today. It has been agriculturally hybrid, not genetically lab engineered over some decades to resist fungus, grow more quickly, and be more pliable for industrial bread baking. As a consequence, 50-60 years ago wheat containing only five percent gluten has become 50 percent gluten today.

Agricultural resources used the hybrid process for wheat to accommodate the baking industry’s mechanical requirements of pliable proteins, leading to the 10-fold increase of wheat’s gluten.

The processed food industry’s concern for production efficiency and perception of consumer demands has focused on the bottom line with the usual disregard to negative health consequences.

Slightly different high speed methods of baking evolved over time. By artificially bleaching flour and adding “improvers” with often toxic additives and mixing the dough violently, loaves of bread could be baked, cooled, and packaged within a few, short hours. Cheap, unhealthy foods for many with massive profits for a few.

This is beginning to change with measures that seem to offset gluten’s damage for some. For example, Whole Foods has their own bakery providing fresh breads daily without bromides, which can displace the thyroid gland’s iodine contents and create hypothyroidism.

Other local bakeries may provide sprouted grain and real sourdough breads, which even some celiac sufferers manage to consume without adverse reactions.

 

Source:  hungryforchange.tv

Protein could reverse the aging process

protein that could reverse the aging process

protein that could reverse the aging process

Researchers from the Harvard Stem Cell Institute (HSCI) have shown that injections of a protein dubbed GDF11, when administered to older mice, appear to cause a reversal of many signs of aging. Analysis showed that every major organ system tested displayed signs of improvement, with the protein even appearing to reverse some of the DNA damage which is synonymous with the aging process itself.

The protein GDF11 is found in humans as well as mice, and is now being considered for possible human testing due to its surprising and apparently regenerative properties.

A previous study had focused on examining the hearts of mice the equivalent of 70 human years old. The mice were regularly exposed to the blood of younger mice whose blood carried a higher concentration of GDF11. Ordinarily the hearts of older mice are enlarged and weakened, however results from the previous study displayed that, thanks to the GDF11 protein present in the blood of the younger mice, the hearts of the elderly mice reduced in size, making them appear younger and healthier. The changes were not purely aesthetic however, with the mice displaying an increased ability to exercise for prolonged periods of time.

The most recent set of experiments tested the protein in two ways. The first stage of the testing involved linking the circulatory systems of an older and a younger mouse through what is known as a parabiotic system. This allowed the protein-rich blood from the younger mouse to flow through the elder’s system continuously, maximizing the effect of the protein. The second method involved injecting the older mice with a concentrated dose of GDF11.

Results from the second study showed that the protein had positive effects reaching far beyond the heart. It was found that, having been exposed to increased levels of the protein, all organs examined by the researchers displayed a heightened level of function. Furthermore, whilst previous studies on the protein had focused on regenerating damaged muscle in mice, the most recent study focused on the repair of cells damaged by the aging process. The GDF11 protein was found to reverse some of this damage, allowing muscle to function as effectively as that of a much younger mouse.

Analysis of the brains of the older mice via MRI imaging displayed an increase in neural stem cells along with the development of blood cells in the brain. “There seems to be little question that, at least in animals, GDF11 has an amazing capacity to restore aging muscle and brain function,” states Dr. Doug Melton, co-chair of HSCI. The team believes that due to the increased blood flow exhibited in the brain of the elderly mice, it may be possible to reverse some of the cognitive effects of aging. The protein was also found to improve the olfactory system of older mice, greatly heightening their sense of smell.

In terms of human applications, it is hoped that a drug derived from GDF11 will lead to a cure for conditions such as diastolic heart failure. This condition is a defect which eventually causes one or more of the ventricles of the heart to deteriorate while attempting to fill the heart with blood, in order to pump it around the body. There is also a possibility that a GDF11-inspired drug could be used to combat Alzheimer’s, a condition synonymous with the aging process.

Looking to the future, the team will continue studies of the GDF11 protein, with a view to begin human medical trials within three to five years.

 

Source: w.gizmag.com

Protein Drug mimic’s food deprivation

A Drug That Can Extend Life as Effectively As Dieting:

A Drug That Can Extend Life as Effectively As Dieting

A Drug That Can Extend Life as Effectively As Dieting

Many studies have shown that rigorous caloric restriction, or strict dieting, can increase longevity dramatically in lifeforms from yeast to humans. But a study released today shows one way to mimic the life-extending effects of food deprivation – using drugs.

A team of researchers in the UK explored the role of a protein known as S6K1, which turns out to play an extraordinary role in aging and age-related disease. When the researchers grew mice lacking the gene to produce S6K1, their mice lived significantly longer (see chart – the red lines are mice without S6K1). They also developed fewer age-related debilitating conditions.

A Drug That Can Extend Life as Effectively As Dieting

Female mice without S6K1 lived slightly longer than their male counterparts, and over 160 days longer than the control group. That means the female mouse lifespan increased by twenty percent.

Mice without S6K1 also lost weight, even if they ate more than ordinary mice. In other words, a substance that could block the expression of S6K1 would trick the body into thinking that you’d gone on a very rigorous diet. And it would make you healthier into an older age. The best part?

In their paper, the researchers conclude:

It might be possible to develop drug treatments that manipulate S6K1 and AMPK to achieve improved overall health in later life. Indeed, short-term rapamycin treatment reduces adiposity in mice, and metformin treatment [often used against type 2 diabetes] extends lifespan in short-lived mice.

This is good news, because often when researchers make discoveries related to longevity there is no immediate pathway to manufacturing a life-extending drug. For all of us who want to stay healthy in old age while still eating sugar and fat once in a while, let’s hope this research team starts testing a drug based on their S6K1 discovery – and soon.