An ingredient found in the natural supplement green tea may help treat brain diseases such as Alzheimer’s, Huntington’s and Parkinson’s.

According to a study published in Natural Chemical Biology, mixing EGCG, a green tea ingredient, with the chemical DAPH-12 may help destroy amyloids—proteins that can lead to brain diseases.

Some feel this study is significant as no other research has found a chemical combination to destroy amyloids. Researchers found that while EGCG could destroy weaker amyloids on its own, it needed to be mixed with DAPH-12 to destroy the stronger proteins.

While the researchers said they were excited with the outcome of finding a potential way to treat the diseases, they are quick to point out there is still more research to be done to see if they could find other possible solutions.

“Our findings are certainly preliminary and we need further work to fully comprehend the effects of EGCG in combination with other chemicals on amyloids,” said co-author Dr. Martin Duennwald. “Yet, we see our study as a very exciting initial step toward combinatorial therapies for the treatment of amyloid-based diseases.”

A new study has found a derivative of cholesterol is necessary for brain cell formation.

Researchers at Sweden’s Karolinska Institute say tests on mice prove that the formation of dopamine-producing neurons during brain development is dependent on the activation of a specific receptor in the brain by an oxidized form of cholesterol called oxysterol.

Dopamine-producing nerve cells play an important part in many brain functions and processes, from motor skills to reward systems and dependency. They are also the type of cell that die in Parkinson’s disease.

In addition, oxysterol was helpful in creating more dopamine-producing nerve cells in laboratory-cultivated embryonic stem cells. “It is a great advancement since it increases the possibility of developing new treatments for Parkinson’s disease,” said Professor Ernest Arenas of the Karolinska Institute.

Researchers say their findings are important for the future of Parkinson’s disease research and treatments. They hope it will be possible to replace dead cells in the brains of Parkinson’s patients with transplanted cultivated dopamine-producing cells. Such cells can also be used to test new Parkinson’s drugs.

According to the Mayo Clinic, nutritional supplements and therapies have also been helpful in treating the symptoms of Parkinson’s. Simple physical activities such as walking and swimming as well as physical therapy and soothing massage can provide relief from muscle rigidity and have other neuromuscular benefits.

“The disease is currently diagnosed by tremors at rest and stiffness in the body and limbs,” said Xuemei Huang, associate professor of neurology, Penn State Hershey College of Medicine. “But by the time we diagnose the disease, about 50 to 80 percent of the critical cells called dopamine neurons are already dead.”

Huang and her colleagues are studying gait, or the manner in which people walk, to understand the physical signs that might be a very early marker for the onset of Parkinson’s. They have confirmed Huang’s clinical impression that in people with Parkinson’s, the arm swing is asymmetrical. In other words, one arm swings much less than the other as a person walks.

“We know that Parkinson’s patients lose their arm swing even very early in the disease but nobody had looked using a scientifically measured approach to see if the loss was asymmetrical or when this asymmetry first showed up,” said Huang. Her team’s findings appear in the current issue of Gait and Posture. “Our hypothesis is that because Parkinson’s is an asymmetrical disease, the arm swing on one arm will be lost first compared to the other.”

The researchers compared the arm swing of 12 people diagnosed three years earlier with Parkinson’s, to eight people in a control group. The Parkinson’s patients were asked to stop all medication the night before to avoid influencing the test results.

The team used special equipment to measure movement accurately, including many reflective markers on the study participants and eight digital cameras that captured the exact position of each segment of the body during a walk.

“Images from the cameras were sent to a computer where special software analyzed the data” explained Huang. “When a person walks, the computer was able to calculate the degree of swing of each arm with millimeter accuracy.”

Analysis of the magnitude of arm swing, asymmetry and walking speed revealed that the arm swing of people with Parkinson’s has remarkably greater asymmetry than people in the control group — one arm swung significantly less than the other in the Parkinson’s patients.

When the participants walked at a faster speed, the arm swing increased but the corresponding asymmetry between them remained the same.

“We believe this is the first demonstration that asymmetrical arm swings may be a very early sign of the disease,” said Huang.

While slightly irregular arm swing occurs in people without Parkinson’s, the asymmetry is significantly larger in those suffering from the disease.

“Our data suggests that this could be a very useful tool for the early detection of Parkinson’s,” noted Huang. “There are wide scale efforts to find drugs that slow cell death. When they are found, they could be used in conjunction with this technique to arrest or perhaps cure the disease because they could be given before great damage has occurred.”

According to a study published in Natural Chemical Biology, when EGCG, a green tea ingredient mixed with chemical DAPH-12, it may help destroy amyloids, which are proteins that bring on the brain diseases.

Some feel this study is significant as no other research has found a chemical combination to destroy amyloids. Researchers found that while EGCG could destroy weaker amyloids on their own, it needed to be mixed with DAPH-12 to destroy the stronger proteins.

While the researchers said they were excited with the outcome of finding a potential way to treat the diseases, they are quick to point out there is still more research to be done to see if they could find other possible solutions.

“Our findings are certainly preliminary and we need further work to fully comprehend the effects of EGCG in combination with other chemicals on amyloids,” said co-author Dr. Martin Duennwald. “Yet, we see our study as a very exciting initial step towards combinatorial therapies for the treatment of amyloid-based diseases.”

Assistant Professor Hiro Furukawa, Ph.D., and colleagues at CSHL, in cooperation with the National Synchrotron Light Source at Brookhaven National Laboratory, obtained crystal structures for one of several “subunits” of the NMDA receptor. This receptor, formally called the N-methyl-D-aspartate receptor, belongs to a family of cellular receptors that mediate excitatory nerve transmission in the brain. Excitatory signals represent the majority of nerve signals in most regions of the human brain.

One theory of causation in Alzheimer’s, Parkinson’s and multiple sclerosis posits that excessive amounts of the excitatory neurotransmitter, glutamate, can cause an overstimulation of glutamate receptors, including the NMDA receptor. Such excitotoxicity, the theory holds, can cause nerve-cell death and subsequent neurological dysfunction. A class of inhibitors of the NMDA receptor under the generic name Memantine has been approved by the U.S. Food and Drug Administration for use in moderate and severe cases of Alzheimer’s.

Memantine is a non-specific inhibitor of the NMDA receptor and is neither a cure nor an agent that can halt progression of the disease. The search is well under way for molecules that can shut down the NMDA receptor with much greater specificity. The CSHL team’s work pertains directly to that effort. The NMDA receptor is modular, composed of multiple domains with distinct functional roles. Part of the receptor is lodged in the membrane of nerve cells and part juts out from the membrane. Furukawa’s CSHL team focused on a portion of the so-called extracellular domain of the receptor, a subunit called NR2B, which includes a domain of particular interest called the ATD (the amino terminal domain).

“This part is of great interest to us because it has very little in common with ATDs in other kinds of glutamate receptors involved in nerve transmission,” says Furukawa. Its uniqueness makes it a potentially interesting target for future drugs. “Our interest is even keener because we already know there are a rich spectrum of small molecules that can bind the ATD of NMDA receptors.” Without a highly detailed molecular picture of the ATD, however, efforts to rationally design inhibitors cannot proceed.

Hence the importance of Furukawa’s achievement: a crystal structure revealed by the powerful light source at Brookhaven National Laboratory, that shows the ATD to have a “clamshell”-like appearance that is important for its function. The results are published in a paper appearing online Thursday ahead of print in The EMBO Journal, the publication of the European Molecular Biology Organization. The team obtained structures of the ATD domain with and without zinc binding to it.

Zinc is a natural ligand that docks at a spot within the “clamshell” in routine functioning of the NMDA receptor. Of much greater interest is the location and nature of a suspected binding site of a small molecule type that is known to bind the ATD and inhibit the action of the NMDA receptor.

These inhibitor molecules are members of a class of compounds called phenylethanolamines which “have high efficacy and specificity and show some promise as neuroprotective agents without side effects seen in compounds that bind at the extracellular domain of other receptors,” Furukawa explains.

Now that his team has solved the structure of the ATD domain of the NR2B subunit, it becomes possible to proceed with rational design of a phenylethanolamine-like compound that can precisely bind the ATD within what Furukawa and colleagues call its “clamshell cleft,” based on the crystal structure they have obtained.

Many of the pesticides studied are still used in Britain, while those which have been banned can remain in the body for decades, previous research has shown.

Although the latest findings looked at exposure to the chemicals through work, earlier studies have suggested that damage could be caused even by small amounts of exposure to the chemicals.

Overall, the study found that those whose job involved using pesticides were 80 per cent more likely to develop the condition, which affects 120,000 people in Britain.

However, exposure to any of three chemicals, a weedkiller called 2,4-dichlorophenoxyacetic acid, or 2,4-D, an insecticide called permethrin, or another weedkiller called paraquat, increased the risk three-fold.

In laboratory tests the pesticides have been shown to destroy cells that release a chemical called dopamine, which carries messages around the brain and helps to control the movement of muscles.

Although paraquat was banned by the European Union in 2007, the other two are still available for use in Britain.

The Royal Horticultural Society even recommends products containing 2,4-D, which include Supergreen Feed, Weed and Mosskiller, for use to kill some weeds.

Permethrin is used to kill insects and pests and in 2007 the Veterinary Poisons Information Service Exposure warned that powerful dog flea treatments which contained the chemical were being wrongly given to cats, inadvertently killing hundreds of them.

The study, by a team from the Parkinson’s Institute, in Sunnyvale, California, asked 519 patients with the disease and 511 healthy people about their jobs and exposure to a range of chemicals.

In total 44 of the patients with Parkinson’s and 27 of the healthy volunteers had been exposed to pesticides through their occupation.

Other occupations, including painting and welding, did not increase the risk of developing Parkinson’s.

The study also found that people who had worked in agriculture but who had not been exposed to pesticides through their work were no more likely to develop the disease.

Writing in the Archives of Neurology journal the researchers say that while they did not look at pesticide exposures such as hobby gardening or residential exposure, “because these exposures may affect many more subjects, future attention is warranted.”

Campaigners claimed that millions more who lived near sprayed fields could be at risk.

Georgina Downs, who took a case against pesticides to the High Court last year, said: “Although the findings of this study are related to occupational exposure the authors acknowledge that other sources of exposure may affect many more subjects.

“There are potentially millions of rural residents throughout the country who live in the locality to pesticide sprayed fields and who are subjected to repeated exposures to “cocktails” of pesticides throughout every year and in many cases for decades.”

Dr Kieran Breen, Director of Research at the Parkinson’s Disease Society (PDS) said that there was “growing evidence” of a link between pesticides and Parkinson’s.

However, he added that a recent survey of sufferers had shown that only nine per cent of them had had long term exposure, of more than one year, to pesticides or herbicides.

He said: “This shows that whilst pesticides may well be contributing to nerve cell death in some people with Parkinson’s, they are unlikely to be the only cause.”

Earlier this year a study found that Parkinson’s sufferers tended to have higher levels of another banned chemical, called Lindane, in their body than other people.

Researchers said that chemical could act as a “trigger” to people already prone to develop the disease.

Parkinson’s occurs when nerve cells in the part of the brain that controls muscle movement become damaged or die.

Sources: telegraph.co.uk/health