Parkinson’s disease possibly originates in gastrointestinal tract

Parkinson’s disease has been attributed the clumping together of a protein called alpha-synuclein that are generally found at the ending of the nerve cells. When the protein clumps together, the nerve cells get damaged and it deteriorates the dopamine system and results in issues with movement and speech.

New research suggests that Parkinson’s disease may start off in the gut. The study was conducted on mice and it confirms the theory that the abnormally folded alpha-synuclein may originate in the gut and then eventually spread to the brain. This transmission happens through the vagus nerve, a nerve bundle that sends signals to and from the brain to several of the body’s organs, including the gut, reported recently.

“It supports and really provides the first experimental evidence that Parkinson’s disease can start in the gut and go up the vagus nerve,” said a professor of neurology and co-author of the research.

The research also discovered that the folding of the protein has similar effects on the brain of mice as well as humans, and the symptoms it causes in both are similar. “We have what we think is a really accurate [animal] model that can be used to work out mechanisms – but also to test therapies,” said the Prof.

The Prof. reckoned the possibility of undoing the misfolds in the protein at the gut itself to stop Parkinson’s disease early on. Another reason the researchers believe that the disease origins in the gut is because those who had an appendicitis surgery early in life had a reduced risk of developing Parkinson’s disease later in life.

Through this experiment on mice, they also recorded a drop in dopamine levels in mice. It resulted in the progressive loss of neurons for seven months. The mice also showed a significant deterioration on their motor skills and also developed memory, behavioural and anxiety issues.

Through this research, it was discovered that when the proteins in the gut becomes misfolded, it results in a domino effect that led to the misfold of the same alpha-synuclein protein in the brain as well.

“This study adds support to a growing base of evidence [implying] that changes in the gut play a key role in the initiation of Parkinson’s, although it is not believed to be the only place where the condition may start,” said a Dr.

“By identifying and halting these changes before they reach the brain, we may be able to prevent the majority of Parkinson’s symptoms ever appearing and improve the lives of people who will be affected,” she concluded.

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Huntington's disease attacks and destroys brain cells in humans

Recent study conducted on mice has given more insight into how and why Huntington's disease attacks and destroys certain brain cells in human beings. We're excited about this result because it may explain why the patient gets the disease in this area of the brain called the striatum, said one of the researcher.

According to the study, a toxic protein linked to Huntington's disease can move from neuron to neuron through a nanotube tunnel whose construction is initiated by a protein called Rhes.

People with Huntington's disease inherit a damaged protein that is somehow complicit in destroying brain cells. Scientists discovered this protein in 1993 but are still piecing together its role in this degenerative disease.

Scans show Huntington's disease brains are shrunken and degraded. As the neurons deteriorate, people lose motor control, they can have emotional problems and their thinking and memory suffer.

Symptoms usually begin around age 30-40 and last 15-20 years until death. A rarer and more aggressive form of the disease affects children, cutting their childhood and lives short. About three to seven people out of 100,000 have the disease and it has mostly affected those with European ancestry.
However, the researcher believed the disease is under-reported in other areas. There is a lot of stigmas associated with the disease, he said. In the case of Huntington's the question is can we block this transport and does it have any benefit or effect? he asked.

For this study, the researchers, looked at mouse neurons under a confocal microscope and saw that the cells formed sticky, string-like protrusions around 150 microns long which floated above the cells, connecting them.

When I saw Rhes, making these tunnel-like tubes between the cells I was excited and at the same time perplexed, he said. They may have been missed before because they're on a different plane. You've to be really looking for it. It's like a bridge over a lake. If you're on the lake, you may not see the bridge above, but if you're on the shore, you can see the bridge, he said.

Scientist first described another type of tunneling nanotube in rat neurons in 2004. Since then, a number of researchers have observed them in cancer and other types of cells. But how they form and what they do was less clear.

To find out, the researchers tracked cell cargo moving through this tunnel bridge. They inserted the Huntington's human disease protein into the mouse brain cells, tagged it with fluorescence and then watched as it crossed over and crawled up to enter the neighbouring cell. Once the tunnel delivered it shipment it released and sprang back. Lysosomes and endosomes, cellular cargo bins that transport cell pieces or waste, also travel these inter-cellular highways, he said.

The Rhes protein exists in both mouse and human brains sick with Huntington's disease. Knocking out the Rhes gene in diseased mice results in less brain damage. In a 2009 study, he found that Rhes also alters the Huntington's disease protein's structure making it more toxic to brain cells.

The Rhes protein makes its own road. That is what is surprising to us. But it not only transports itself. Once the road is made, many things can be transported, he said.

The researchers continue to investigate what other proteins may be helping with tunnel construction and if other disease proteins move along these membranous highways. His laboratory is also developing ways to identify how Huntington's disease protein travels in the live brain.

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Rheumatology- All That One Nees To Know

A rheumatologist is a medical doctor that specializes in diseases of the joints, in other words, they specialize in arthritic problems. Rheumatology is noted for its diagnosis and treatment of systemic, autoimmune and inflammatory forms of arthritis. Rheumatologists treat joint diseases in a similar way to orthopedists, but they don’t actually perform surgery. Some 54.4 million are affected by rheumatic diseases in the United States, according to the doctors. It strikes people of both genders and occurs in people of all races and ages. Some 300,000 children in the United States are afflicted by a rheumatic disease.

Although it isn’t every rheumatic disease that affects the spine, the ones that do can be extremely difficult to live with. The most common is osteoarthritis, which occurs when both the cartilage and bone begin to deteriorate.
Another group of rheumatic conditions that affect the spine includes spondyloarthropathies. It includes inflammatory conditions such as ankylosing spondylitis and axial spondylitis. Some types of spondyloarthropathies also affect the joints.
Ankylosing spondylitis, for example, affects the lower back most, but it can also affect hips, shoulders, and knees. Psoriatic arthritis can affect the spine, but it doesn’t in certain instances. With that being said, it always tends to affect the ends of fingers and toes. These are just two types of spondyloarthropathy that exist which are capable of damaging the spine as well as other areas of the body.

You should see a rheumatologist when your joints hurt, or if there are signs of inflammation such as redness, swelling, pain, stiffness, and loss of joint function that lasts for two days or more. You’ll likely need to see your primary care doctor before seeing a rheumatologist for a referral. Keep in mind that the earlier you see your primary care doctor, the sooner your ailment can be treated.
The rheumatologist warns that autoimmune disorders and rheumatic diseases actually run in families. If your family members, regardless of whether they are immediate family member or not, have or had an autoimmune disorder or rheumatic disease, then you should definitely see a rheumatologist sooner rather than later.
Note that medications given to you by your primary care doctor will temporarily improve things, but that doesn’t mean that your symptoms won’t return. If this occurs, then you also need to see a rheumatologist.

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To Be Mentally Healthy Eat a Low-Protein, High-Carb Diet

The key to a long life and a healthy brain, according to a study, is a low-protein, high-carbohydrate diet. This study, shows improvements in overall health and brain health, as well as learning and memory, among mice fed an unrestricted low protein, high carbohydrate diet. 

 

Lead author says, "There are currently no effective pharmaceutical treatments for dementia – we can slow these diseases, but we can't stop them – so it's exciting that we are starting to identify diets that are impacting how the brain ages."

For the first time, research shows that unrestricted low-protein, high carbohydrate diets have similar protective benefits for the brain as calorie restriction, which is known for its longevity benefits, but it is not sustainable in humans. "We have close to 100 years of quality research extolling the benefits of calorie restriction as the most powerful diet to improve brain health and delay the onset of neurodegenerative disease in rodents," says the author.

"However, the majority of people have a hard time restricting calories, especially in Western societies where food is so freely available. It shows a lot of promise that we have been able to replicate the same kind of gene changes in the part of the brain responsible for memory that we also see when we severely restrict calories."

According to Senior author, numerous cultures including those who live long lives in Okinawa in Japan, and many parts of the Mediterranean have long observed this mix. In Okinawa, around 9% of protein comes from lean fish, soy and plants, with very little beef. One of their main sources of carbohydrates is sweet potato.

In the current study, researchers fed the mice complex carbohydrates derived from starch and casein protein, which is found in cheese and milk. This assessed the brain benefits of the diet. The researchers focused on the hippocampus - this region of the brain is responsible for learning and memory. The Prof. says "The hippocampus is usually the first part of the brain to deteriorate with neurodegenerative diseases like Alzheimer's. However, the low-protein high-carbohydrate diet appeared to promote hippocampus health and biology in the mice, on some measures to an even greater degree than those on the low-calorie diet." 

This latest research follows a 2015 study  showed that a low protein, high carbohydrate diet could be just as effective as a low-calorie diet in promoting a long life in mice through good heart and digestive health.

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Cognitive behavioural therapy could treat anxiety in COPD patients

Treating chronic obstructive pulmonary disease (COPD) patients for anxiety using cognitive behavioural therapy (CBT) may reduce hospital visits, finds a study. The findings have been published in a journal.

COPD is a long-term condition that causes inflammation in the lungs, narrowing of the airways and damaged lung tissue, making breathing difficult. Anxiety often occurs alongside COPD and can mean that patients do a less physical activity, leading to loss of fitness, isolation, and deteriorating health overall.

The new study found that brief CBT sessions with respiratory nurses reduced feelings of anxiety for patients with COPD and resulted in the less frequent use of hospital services.

The lead researcher of the study, explained: "One of the main symptoms of COPD is breathlessness. This is very frightening and often leads to feelings of anxiety. Many healthcare professionals do not currently screen COPD patients for symptoms of anxiety, even though it can have an impact on their overall health."

"Feeling anxious has a negative impact on patients' quality of life and leads to the more frequent use of healthcare resources. We wanted to test whether one-to-one CBT sessions delivered by respiratory nurses could reduce symptoms of anxiety and whether this could be a cost-effective intervention." 

The researchers found that CBT was more effective in reducing anxiety symptoms in COPD patients compared to leaflets alone.

After checking the hospital attendance records of patients in the study, the researchers found that for each patient who attended CBT, there was an average saving of £1,089 (approx. Rs. 98,000) for hospital admissions and £63 (approx. Rs. 5,000) for emergency room attendances.

The data also showed no link between a patients' lung function, measured by how much air a person can breathe out in one second, and their anxiety score. The researchers say this suggests that even patients with mild COPD can feel extremely anxious, and so would benefit from this intervention.

Dr. said: "We found that one-to-one CBT sessions delivered by respiratory nurses could reduce symptoms of anxiety and that this could be a cost-effective intervention. Although the CBT intervention initially resulted in added costs, as respiratory nurses required training in CBT skills, this was balanced by the savings made thanks to less frequent need of a hospital."

"Reducing the levels of anxiety patients experience has a significant impact on their quality of life as well as their ability to keep physically active and may improve survival in the long-term. Our research shows that front-line respiratory staff can deliver this intervention efficiently and effectively." 

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Type 2 diabetes drug can exhaust insulin-producing cells, claims new study

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Long-term use of liraglutide - a drug used to lower blood sugar levels in type 2 diabetes patients - may have a deteriorating effect on insulin-producing beta cells, leading to an increase in blood sugar levels, a new study has claimed.

There is now compelling evidence that liraglutide therapy is efficacious at least in the short term, since it produces an initial reduction in blood sugar. However, many patients do not respond to the treatment and some even display adverse reactions such as nausea, vomiting and diarrhoea.

Researchers from Karolinska Institute in Sweden and University of Miami in US conducted a study on mice implanted with human insulin-producing cells. Blood-sugar suppressors in the form of analogues of the incretin hormone GLP-1 are commonly used in the treatment of type 2 diabetes, since they stimulate the glucose response of the pancreatic beta cells to make them secrete more insulin.

To study the long-term effects of incretin therapy, researchers worked with humanised mice, generated by transplanting human insulin-producing cells into the anterior chamber of the eye. The mice were given daily doses of liraglutide for more than 250 days, during which time the researchers were able to monitor how the pancreatic beta cells were affected.

The results showed an initial improvement in the insulin-producing cells, followed by a gradual exhaustion, with reduced secretion of insulin as a response to glucose. This, they say, was unexpected.

"Given the lack of clinical studies on the long-term effect of these drugs in diabetes patients, this is a very important discovery," said Midhat Abdulreda from University of Miami. "We also need to take these results into account before prescribing blood-sugar suppressing GLP-1 analogues when planning long-term treatment regimens for patients," said Per-Olof Berggren from Karolinska Institute.

"Our study also shows in general how to carry out in vivo studies of the long-term effects of drugs on human insulin-producing cells, which should be extremely important to the drug industry," said Berggren.

The findings were published in the journal Cell Metabolism.

Probiotics prevent deadly complications of liver disease: Study

Probiotics are effective in preventing hepatic encephalopathy in patients with cirrhosis of the liver, according to a study by the Govind Ballabh Pant Hospital, New Delhi.


Hepatic encephalopathy is the deterioration of brain function - a serious complication of liver disease.
The research shows that probiotics modify the gut microbiota to prevent hepatic encephalopathy.
According to experts, the results offer a safe, well tolerated and a cheaper alternative to current treatments.

The researchers at G.B. Pant conducted a single-centre, randomised trial with cirrhosis patients who showed risk factors for hepatic encephalopathy, but had yet to experience an obvious episode.
When comparing treatment with probiotics versus placebo, the researchers found that the incidence of hepatic encephalopathy was lower in patients treated with probiotics.

Probiotic supplementation was not associated with any side effects and none of the patients required discontinuation of therapy.

“These results suggest that probiotics are similar in effectiveness to the current standard of care, lactulose, in the prevention of hepatic encephalopathy, yet they appear to be much better tolerated,” researchers added.

Up to 45 percent of patients with cirrhosis develop hepatic encephalopathy, a loss of brain function that occurs when the liver is unable to remove toxins from the blood.

Prognosis is poor, with a 58 percent mortality rate at one year, and a 77 percent mortality rate at three years.

"These results offer a safe, well tolerated and perhaps cheaper alternative to current treatments," said David W. Victor III, who contributed an editorial in the journal Clinical Gastroenterology and Hepatology on this research.

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