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Eating more fish could prevent Parkinson's disease.

A new study from Chalmers University of Technology, Sweden, shines more light on the link between consumption of fish and better long-term neurological health. Parvalbumin, a protein found in great quantities in several different fish species, has been shown to help prevent the formation of certain protein structures closely associated with Parkinson's disease.

Fish has long been considered a healthy food, linked to improved long-term cognitive health, but the reasons for this have been unclear. Omega-3 and -6, fatty acids commonly found in fish, are often assumed to be responsible, and are commonly marketed in this fashion. However, the scientific research regarding this topic has drawn mixed conclusions. Now, new research from Chalmers has shown that the protein parvalbumin, which is very common in many fish species, may be contributing to this effect.

One of the hallmarks of Parkinson's disease is amyloid formation of a particular human protein, called alpha-synuclein. Alpha-synuclein is even sometimes referred to as the 'Parkinson's protein'. What the Chalmers researchers have now discovered, is that parvalbumin can form amyloid structures that bind together with the alpha-synuclein protein. Parvalbumin effectively 'scavenges' the alpha-synuclein proteins, using them for its own purposes, thus preventing them from forming their own potentially harmful amyloids later on.

"Parvalbumin collects up the 'Parkinson's protein' and actually prevents it from aggregating, simply by aggregating itself first," explains Pernilla Wittung-Stafshede, Professor and Head of the Chemical Biology division at Chalmers, and lead author on the study. With the parvalbumin protein so highly abundant in certain fish species, increasing the amount of fish in our diet might be a simple way to fight off Parkinson's disease. Herring, cod, carp, and redfish, including sockeye salmon and red snapper, have particularly high levels of parvalbumin, but it is common in many other fish species too. The levels of parvalbumin can also vary greatly throughout the year. "Fish is normally a lot more nutritious at the end of the summer, because of increased metabolic activity. Levels of parvalbumin are much higher in fish after they have had a lot of sun, so it could be worthwhile increasing consumption during autumn," says Nathalie Scheers, Assistant Professor in the Department of Biology and Biological Engineering, and researcher on the study. It was Nathalie who first had the inspiration to investigate parvalbumin more closely, after a previous study she did looking at biomarkers for fish consumption.

Other neurodegenerative diseases, including Alzheimer's, ALS and Huntington's disease, are also caused by certain amyloid structures interfering in the brain. The team is therefore keen to research this topic further, to see if the discovery relating to Parkinson's disease could have implications for other neurodegenerative disorders as well. Pernilla Wittung-Stafshede stresses the importance of finding ways to combat these neurological conditions in the future: "These diseases come with age, and people are living longer and longer. There's going to be an explosion of these diseases in the future -- and the scary part is that we currently have no cures. So we need to follow up on anything that looks promising."

A follow up study, looking at parvalbumin from another angle, is indeed planned for this autumn. Nathalie Scheers, together with Professor Ingrid Undeland, also of Chalmers, will investigate parvalbumin from herring, and its transport in human tissues. "It will be very interesting to study how parvalbumin distributes within human tissues in more depth. There could be some really exciting results."

More About: Fish and Better Neurological Health

The link between higher consumption of fish and better long-term health for the brain has been long established. There is correlation between certain diets and decreased rates of Parkinson's disease -- as well as other neurodegenerative conditions. "Among those who follow a Mediterranean diet, with more fish, one sees lower rates of Parkinson's and Alzheimer's," says Tony Werner, a PhD student in the Department of Biology and Biological Engineering, and lead researcher on the study. This has also been observed in Japan, where seafood forms a central part of the diet. The team is careful to note that no definite links can be established at this point, however.

More About: Amyloids and Aggregation

Proteins are long chains of amino acids that fold into specific structures to carry out their function. But sometimes, proteins can fold incorrectly, and get tangled up with other proteins, a process known as aggregation. As these misfolded proteins aggregate together, they create long fibrous structures known as amyloids. Amyloids are not necessarily a bad thing, but can be responsible for various diseases. Some of them can interfere with neurons in the brain, killing those cells, and causing a variety of neurodegenerative conditions.

More About: The Study

Nathalie Scheers had looked at parvalbumin before in another context. "I was on a previous study where we looked at possible compliance markers for fish intake. Parvalbumin is a cause of fish allergies, so we knew that it passed over to the blood, and that this form of parvalbumin is specific for fish" She joined forces with Pernilla Wittung-Stafshede, and together they took the idea forward. "Because Nathalie had previously shown that parvalbumin passes into the body of the person eating fish, it made sense to study its interaction with human proteins. We already knew that they can meet in the gut, the blood, or the brain," explains Pernilla Wittung-Stafshede.


Study: Exercise may slow Parkinson’s progression.

Intense treadmill exercise can be safe for people who have recently been given diagnoses of Parkinson’s disease and may substantially slow the progression of their condition, according to an important new study of adults in the early stages of the disease.

But the same study’s results also indicate that gentler exercise, while safe for people with Parkinson’s, does not seem to delay the disease’s advance.

As most of us know, Parkinson’s disease is a progressive neurological disorder that involves problems with motor control. Symptoms like weakness, stiffness, loss of balance and falls can make exercise difficult and potentially hazardous. Though Parkinson’s is currently incurable, its symptoms can be eased for a time with various drugs. But most of those drugs lose their effectiveness in people over time. So some researchers have begun searching for other treatment options, particularly for use in the beginning stages of the disease. If people with early Parkinson’s could brake the disease’s advance and delay their need to start medications, the researchers have reasoned, they might change the arc of their disease, delaying its most severe effects.

That possibility recently led a consortium of researchers from Northwestern University, the University of Colorado’s Anschutz Medical Campus in Aurora and other institutions to look at exercise as a treatment. There were precedents. Animal studies already had shown that exercise reduced symptoms and slowed physical decline in a rodent version of Parkinson’s. But rodents are not people. And while some previous studies in people have shown that cycling (especially on a tandem bike), boxing, dancing and other activities may produce benefits in people with Parkinson’s, other studies had produced inconsistent results. In addition, many of these earlier studies had used many different types and amounts of exercise, and none had systematically compared different varieties of exercise head-to-head.

So for the new study, which was published in JAMA Neurology, the researchers decided to treat exercise as if it were a drug and carefully track the safety and effectiveness of different "doses" of exercise in a formal Phase 2 clinical trial.

In drug research, Phase 1 trials establish the basic safety of a drug in small-scale experiments. Phase 2 studies look at larger groups of people to see if the intervention remains safe and also whether, in the tortured English of pharmacopoeia, it is "nonfutile," meaning that it has enough beneficial effect to deserve further testing.

For this Phase 2 study, the researchers first recruited 128 men and women who had been diagnosed with Parkinson’s within the past five years. None yet were taking medications to treat the disease. None regularly exercised. The researchers tested their aerobic capacity, maximum heart rates and disease severity, using a standard numerical scale. They then divided the men and women randomly into three groups, one of which was asked to continue their normal lives as a control. (For fairness, they were wait-listed for exercise training later.)

The others were assigned to start exercising. One group walked gently for 30 minutes on a treadmill four times a week, while the researchers manipulated the machines’ speed and incline to keep each volunteer’s heart rate at between 60 and 65 percent of his or her maximum. The others exercised for the same amount of time, but at a strenuous pace and incline, so that their heart rates stayed at between 80 and 85 percent of their maximum. For a month, the sessions were supervised. Then the volunteers were asked to continue on their own, with heart rate monitors substantiating their efforts. The researchers asked to be told about any injuries among the volunteers.

Then, at the end of six months, they rechecked the volunteers’ disease status. To no one’s surprise, the men and women who had continued with their previous lives showed some worsening. Their scores on the disease scale had declined on average by more than three points. Likewise those in the moderate exercise group showed declines of around two points, meaning that, by the study’s standards, the exercise had been “futile” as a Parkinson’s treatment. But the group that had worked out intensely showed almost no decline in their disease scores, meaning their exercise had been "nonfutile." It had helped.

Just as important, it had been tolerable. Almost everyone in both exercise groups had managed to complete six months of regular exercise without injuries and with only sporadic complaints of sore muscles.

The study was not designed to determine why intense exercise slowed the progression of Parkinson’s and moderate exercise did not. But "my guess is that high-intensity exercise does a better job at improving brain vascularity and neuronal blood supply," says Daniel Corcos, a professor of human movement sciences at Northwestern University Feinberg School of Medicine who helped to lead the study. Improved blood flow to the brain, the thinking goes, may aid overall brain health and slow deterioration. But that hypothesis will need to be tested, he says.

A larger, longer-term Phase 3 study of intense exercise as a treatment for early Parkinson’s also is needed, he says, and is now justified, based on these results. He and his colleagues are in fact already planning such an experiment. But in the meantime, the results indicate that someone who has recently received a diagnosis of Parkinson’s might consider "an intense exercise program," he says.

Speak with your doctor first, naturally, and perhaps consult an athletic trainer familiar with Parkinson’s. But the findings are encouraging, suggesting that intense exercise is unlikely to be harmful and, in meaningful ways, could help.