Laughter may be the best medicine for age-related memory loss

We are all familiar with the saying, "laughter is the best medicine." And this motto may ring true when it comes to tackling age-related memory loss; a new study from Loma Linda University in California finds that humor may reduce brain damage caused by the "stress hormone" cortisol, which in turn, improves memory.

The research team, led by Dr. Gurinder Singh Bains, recently presented their findings at the Experimental Biology meeting in San Diego.

It is well known that too much stress can negatively affect health. Medical News Today recently reported on a study suggesting that stress may worsen allergies, while other research indicates that it makes the brain more susceptible to mental illness.

Past research has also shown that stress can worsen memory and learning ability in elderly individuals. This is because stress increases production of cortisol - a hormone that can cause damage to neurons in the brain.

Since it is well known that laughter can be a stress reliever, the research team wanted to determine whether humor may reduce brain damage caused by cortisol.

Watching a funny video 'reduced cortisol levels and boosted memory performance'

The researchers analyzed one group of elderly individuals who had diabetes and another group of elderly people who were healthy.

Laughter may reduce neuron damage caused by "stress hormone" cortisol, therefore improving memory in older individuals.

Both groups were required to view a 20-minute humorous video, before completing a memory test that measured their visual recognition, learning ability and memory recall.

A third group of elderly individuals were asked to complete the memory test without watching the funny video. The team then compared the results of all three groups.

Cortisol levels for all participants were recorded before and after the experiments.

The investigators found that both groups who watched the humorous video showed a significant reduction in cortisol levels, compared with the group that did not view the video.

The groups that watched the funny video also showed greater improvement in memory recall, learning ability and sight recognition, compared with those who did not watch the video. The diabetic group demonstrated the greatest improvement in both cortisol levels and memory test scores.

'Laughter may improve memory and quality of life'

Study co-author Dr. Lee Burk says these findings suggests that the less stress a person has, the better their memory performance, and humor may be the key to reducing stress levels.

"Humor reduces detrimental stress hormones like cortisol that decrease memory hippocampal neurons, lowers your blood pressure, and increases blood flow and your mood state," he explains.

"The act of laughter - or simply enjoying some humor - increases the release of endorphins and dopamine in the brain, which provides a sense of pleasure and reward."

He says that these neurochemical changes in the brain also increase "gamma wave band frequency," which can improve memory.

"So, indeed," he adds, "laughter is turning out to be not only a good medicine, but also a memory enhancer adding to our quality of life."

Dr. Bains says the team's findings may offer benefits that can be applied to wellness programs for elderly individuals, adding:

"The cognitive components - learning ability and delayed recall - become more challenging as we age and are essential to older adults for an improved quality of life: mind, body and spirit.

Although older adults have age-related memory deficits, complimentary, enjoyable and beneficial humor therapies need to be implemented for these individuals."

Laughter may not be the only way to boost memory. Medical News Today recently reported on a study suggesting that green tea may improve working memory, while other research from Johns Hopkins University in Maryland found that caffeine may boost long-term memory.

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Dose of measles virus destroys woman's incurable cancer

In what they describe as a proof of principle study, doctors in the US were able to keep a woman with deadly multiple myeloma - an incurable bone marrow cancer - free of all signs of living cancer cells for over 6 months by giving her just one high dose of measles virus.

Two patients received a single intravenous dose of measlesvirus that was engineered to kill myeloma plasma cells and not harm other cells.

The team, from the Mayo Clinic in Rochester, MN, says both patients responded to the treatment, showing reduced bone marrow cancer and levels of myeloma protein.

But one patient, a 49-year-old woman, experienced complete remission and remained disease-free for over 6 months.

A report on this first study to establish the feasibility of the treatment appears in the journal Mayo Clinic Proceedings.

Proof virotherapy works for disseminated cancer

First author Dr. Stephen Russell, hematologist and co-developer of the therapy, says:

"This is the first study to establish the feasibility of systemic oncolytic virotherapy for disseminated cancer. These patients were not responsive to other therapies and had experienced several recurrences of their disease."

The treatment is an example of oncolytic virotherapy - using engineered viruses to fight cancer - an approach that dates back to the 1950s. Thousands of patients have received this type of therapy, using oncolytic viruses from various families, including common cold viruses, herpes viruses and pox viruses.

But the authors say this is the first well-documented case of a patient with cancer that has spread experiencing complete remission at all disease sites after receiving oncolytic virus therapy.

Myeloma is a cancer that develops in plasma cells - a type of blood cell made in the bone marrow. According to the American Cancer Society, the disease is relatively uncommon, and in the US, there is a 1 in 149 risk of developing it.

Myeloma can arise in any part of the body where there is bone marrow, including the spine, rib cage and pelvis. Multiple myeloma means it is occurring in more than one place.

The disease, which also causes skeletal or soft tissue tumors, usually responds to drugs that stimulate the immune system, but it eventually overcomes them and is rarely cured.

First use of highest possible dose of engineered measles virus

Dr. Russell and colleagues explain in their article that they chose to report these two cases in particular because they were the first patients they had studied who had received the highest possible dose, and with limited previous exposure to measles, so their immune systems did not have many antibodies to the virus. They had also exhausted other treatment options.

Senior author Dr. Angela Dispenzieri, an expert in multiple myeloma, says in very simple terms, the measles virus makes the cancer cells join together and explode. The treatment also appears to trigger another lasting benefit:

"There's some suggestion that it may be stimulating the patient's immune system to further recognize the cancer cells or the myeloma cells and help mop that up more effectively than otherwise."

Having effectively completed a phase I clinical trial - to prove the concept that the measles virus can fight cancer - the team is now moving quickly into a phase II trial involving more patients.

They also intend to test the virus's effectiveness as a tool to fight other cancers, such as head and neck, brain and ovarian cancers and mesothelioma. And they are engineering other viruses that may be able to kill cancer cells.

Dr. Russell says they have recently started to think along the lines of "a single shot cure for cancer, and that's our goal with this therapy."

He and two other authors of the study, as well as the Mayo Clinic, have declared a financial interest in the methods used in the study, which was funded by the National Cancer Institute of the National Institutes of Health, Al and Mary Agnes McQuinn, The Harold W. Siebens Foundation and The Richard M. Schulze Family Foundation.

Medical News Today recently reported on a study in Nature Genetics, where scientists from The Institute of Cancer Research in the UK found a gene involved in aging is linked to multiple myeloma. The team said the discovery brings the total genetic variants linked to myeloma to seven and may help establish the genetic causes of the disease.

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Why was 1918 flu pandemic so deadly? Research offers new clue

In 1918, as one global devastation in the shape of World War I came to an end, people around the world found themselves facing another deadly enemy, pandemic flu. The virus killed more than 50 million people, three times the number that fell in the Great War, and did this so much faster than any other illness in recorded history.

But why was that particular pandemic so deadly? Where did the virus come from and why was it so severe? These questions have dogged scientists ever since. Now, a new study led by the University of Arizona (UA) may have solved the mystery.

Michael Worobey, a professor in UA College of Science's Department of Ecology and Evolutionary Biology, and colleagues describe their findings in the Proceedings of the National Academy of Sciences.

They hope the study not only offers some new clues about the deadliness of the 1918 pandemic, but will also help improve strategies for vaccination and pandemic prevention, as Prof. Worobey explains:

"If our model is correct, then current medical interventions, especially antibiotics and vaccines, against several pneumonia-causing bacteria, could be expected to dramatically reduce mortality, if we were faced today with a similar set of pandemic ingredients."

The 1918 pandemic killed predominantly young adults

One of the questions that has been particularly vexing is why the 1918 pandemic human influenza A virus killed so many young adults in the prime of life, he says, adding: "It has been a huge question whether there was something special about that situation, and whether we should expect the same thing to happen tomorrow."

Researchers reconstructed the origins of the 1918 pandemic virus, the classic swine flu and the postpandemic seasonalH1N1 flu virus lineage that circulated between 1918 and 1957, to find out why the 1918 pandemic was so deadly.

Usually, the human influenza A virus is deadlier to infants and the elderly. But the 1918 strain killed many people in their 20s and 30s, who mainly died from secondary bacterial infections, especially pneumonia.

For their investigation, the researchers developed an unprecedentedly accurate "molecular clock," a technique that looks at the rate at which mutations build up in given stretches of DNA over time.

Evolutionary biologists use molecular clocks to reconstruct family trees, follow lineage splitting and find common ancestors of different strains of viruses and other organisms.

Prof. Worobey and his team used their molecular clock to reconstruct the origins of the 1918 pandemic virus, the classic swine flu and the postpandemic seasonal H1N1 flu virus lineage that circulated between 1918 and 1957.

Genetic material from bird flu virus picked up just before 1918

They found that a human H1 virus that had been circulating among humans since around 1900 picked up genetic material from a bird flu virus just before 1918 and this became the deadly pandemic strain.

Exposure to previous strains of flu virus does offer some protection to new strains. This is because the immune system reacts to proteins on the surface of the virus and makes antibodies that are summoned the next time a similar virus tries to infect the body.

But the further away the new strain is genetically from the ones the body has previously been exposed to, the more different the surface proteins, the less effective the antibodies and the more likely that infection will take hold.

This is what the authors suggest happened to the young adults in the 1918 pandemic. In their childhood around 1880 to 1900, they were exposed to a supposed H3N8 virus that was circulating in the population. This virus had surface proteins that were very different from those of the H1N1 pandemic strain. Their immune system would have made antibodies, but they would have been ineffective against the H1N1 virus.

But people born either before or after those decades would have been exposed to a virus much more like the 1918 one and their immune systems were thus better equipped to fight it.

Prof. Worobey notes:

"We believe that the mismatch between antibodies trained to H3 virus protein and the H1 protein of the 1918 virus may have resulted in the heightened mortality in the age group that happened to be in their late 20s during the pandemic."

He says their finding may also help explain differences in patterns of mortality between seasonal flu and the deadly H5N1 and H7N9 bird flu viruses.

The authors suggest perhaps immunization strategies that mimic the often impressive protection that early childhood exposure provides could dramatically reduce deaths from seasonal and new flu strains.

In February 2014, Prof. Worobey and colleagues began challenging conventional wisdom about flu outbreaks, when in the journal Nature, they reported the most comprehensive analysis to date of the evolutionary relationships of flu virus across different host species over time.

Among other things, they challenged the view that wild birds are the major reservoir for the bird flu virus. Instead of spilling over from wild birds to domestic birds, they say the more likely scenario is the other way around - that new strains jump from domestic to wild birds.

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