220CNO14DEC2015
CNO Report 220
Release Date 11 DEC 2015
Draft Report Compiled by
Ralph Turchiano
In This Issue:
1. Magnesium ions show promise in slowing progression of Alzheimer’s disease in mice
2. New discovery: This is why we do not constantly get ill despite viruses and bacteria
3. Gut microbes trigger fat loss in response to cold temperatures
4. Living longer and healthier in mind but not in body
5. Alcohol aromatherapy eases nausea in the ER
6. Migraine triggers may all act through a common pathway
7. Plant compound found in spices and herbs increases brain connections
Public Release: 1-Dec-2015
Magnesium ions show promise in slowing progression of Alzheimer’s disease in mice
New research in The FASEB Journal suggests that magnesium ions may slow the progression of the disease by disrupting the development of amyloid plaques
Federation of American Societies for Experimental Biology
New research published in the December 2015 issue of The FASEB Journal, shows that in mouse models of the disease oral administration of magnesium-L-threonate (MgT) alleviated cognitive decline by suppressing the Aβ deposition in amyloid plaques in an APH-1α/1β-dependent manner. Although questions still remain about how MgT permeates the blood-brain barrier, the work suggests that scientists may have found the key to a new series of Alzheimer’s disease treatments. Specifically, they show that magnesium ions target pharynx defective (APH)-APH-1α/1β-suppressing the A? deposition in amyloid plaques in an anterior pharynx defective (APH)-APH-1α/1β-dependent manner.
“We hope that our findings will help improve clinical practice pertinent to the optimal administration of Mg2+ for delaying or even preventing the onset of AD,” said Pu Wang, Ph.D., a researcher involved in the work from the Department of Life Science and Health at Shenyang, Liaoning, China. “Moreover, we hope to extend our experimental models to other disorders such as severe craniocerebral injury, bronchial asthma, chronic pulmonary heart disease, arrhythmia and myocardial necrosis, etc. and identify more targets of Mg2+ and strategies for treating these disorders.”
To make this discovery, Wang and colleagues used two groups of mice. The first group consisted of normal mice. The second group consisted of mice overexpressing a gene that enhances the expression of APH-APH-1α/1β and the production of Aβ, while also decreasing the Mg2+ influx in the brain, especially in cerebrospinal fluid. When researchers restored Mg2+ in the cerebrospinal fluid of the genetically modified mice, the highly induced APH-APH-1α/1β expression was inhibited, which resulted in alleviating Aβ aggregation and cognitive decline. Although the researchers did not find any direct evidence showing that MgT was able to penetrate the blood brain barrier, their findings showed elevated levels of Mg2+ in the brains of the genetically modified mice–sufficient for inhibiting the development of Alzheimer’s disease.
“The good news about this work is that if it holds up in humans, magnesium is a common element that is readily available,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “The bad news, of course, is that what works in mice does not always turn out so well in people. At the same time, even if magnesium ions do not work out for people with Alzheimer’s, this report will help researchers learn how to slow the development amyloid plaques, a hallmark of the disease.”
Public Release: 1-Dec-2015
New discovery: This is why we do not constantly get ill despite viruses and bacteria
Aarhus University
New research breaks with existing knowledge about how our immune system works. Experiments at Aarhus University have shown how the body mobilises a hitherto unknown defence against viruses and bacteria. This also explains why we do not constantly get ill despite the viruses around us.
Fever, sore muscles and other influenza-like symptoms are typical signs that your immune system is fighting against viruses and bacteria. The unpleasant condition is, among other things, due to the body forming a substance called interferon, which must defeat the virus. For many years researchers and doctors have assumed that this was the body’s earliest response when attacked by various infections.
But new research shows that the body’s very first defence mechanism is not interferon, but rather a hitherto unknown mechanism, which begins working even earlier.
The newly discovered immune reaction is activated when the body’s mucous membranes are disrupted, as they are when viruses and bacteria attempt to establish an infection. The immune system recognises the virus and produces a substance that neutralises the uninvited guest. The process goes on continuously without us being aware of it. If this first immune reaction is not sufficient to suppress the virus, the infection establishes itself in the body. This in turn triggers the next reaction involving interferon, which not only helps to fight the virus, but also means we become ill.
The discovery has just been published in the scientific journal Nature Immunology.
Alters our understanding of the immune system
The discovery alters the way in which researchers and doctors previously understood the immune system.
“Our study fundamentally alters our understanding of how the body begins its defence against viruses. This can help to explain how we can be constantly exposed to the viruses and bacteria that always surround us, without activating the entire immune system every time, something that would lead to more frequent influenza-like symptoms,” says Soren Riis Paludan, professor at the Department of Biomedicine at Aarhus University.
He has headed the research project in Aarhus, while also collaborating with researchers from the University of Copenhagen as well as from universities in the USA and Germany.
May explain serious diseases
Experiments on mice have shown that mice, lacking this first defence mechanism, become ill if they are exposed to herpes virus, while normal mice remain healthy.
“We do not yet know the precise significance of this mechanism, but it may explain why some people become more ill from viral infections such as influenza than others. The same may apply to other viral infections that are initiated on mucous membranes such as HIV and herpes. We will now begin to map out the molecules that are involved. Once we have done this, it will be possible to identify people with defects in the mechanism, just as there is a potential to develop new forms of treatment. At the same time, the mechanism may turn out to have significance also for non-viral diseases, so continued research into this area shows great potential,” says Soren Riis Paludan.
Public Release: 3-Dec-2015
Gut microbes trigger fat loss in response to cold temperatures
Cell Press
Exposure to cold temperatures is known to mimic the effects of exercise, protecting against obesity and improving metabolic health. A study published December 3 in Cell now reveals that the beneficial health effects of cold exposure are mediated in part by gut microbes. The researchers found that cold exposure dramatically alters the composition of intestinal bacteria in mice and that this microbial shift is sufficient to burn fat, improve glucose metabolism, and reduce body weight.
“We provide compelling evidence that gut microbes play a key role in our ability to adapt to the environment by directly regulating our energy balance,” says senior study author Mirko Trajkovski of the University of Geneva. “We are excited about exploring the therapeutic potential of these findings and testing whether targeting some of these microbes could be a promising approach for preventing obesity and related metabolic conditions.”
One potential therapeutic avenue for obesity centers on promoting the formation of good types of body fat known as brown and beige fat. Human infants have large amounts of heat-generating brown fat to protect them from extreme cold, and scientists recently discovered that adult humans also retain brown fat stores consisting mainly of a subtype known as beige fat. Cold exposure or exercise can promote the formation of beige fat, thereby burning stored calories and protecting mammals from hypothermia, obesity, and metabolic problems.
Because gut microbes have been implicated in obesity and related metabolic conditions, Trajkovski and his team suspected that they might also play a role in mediating the positive health effects of cold exposure. In support of this idea, they found that exposure to a cold temperature (6° Celsius, 43° Fahrenheit) for up to 10 days caused a major shift in the composition of gut microbes while preventing weight gain in mice.
The researchers next tested the direct impact of these microbes on metabolic health. To do so, they transplanted the cold-induced gut bacteria into other mice that did not harbor gut microbes because they had been raised in a germ-free environment. The transplanted microbes improved glucose metabolism, increased tolerance to cold temperatures, and caused weight loss in the recipient mice by promoting the formation of beige fat. “These findings demonstrate that gut microbes directly regulate the energy balance in response to changes in the environment,” Trajkovski says.
However, after three weeks of cold exposure, body weight began to stabilize. The researchers suspected that the intestine was absorbing more nutrients from food, counteracting additional weight loss that would otherwise result from higher overall energy expenditure.
In support of this idea, transplantation experiments showed that gut microbes associated with long-term cold exposure caused the intestine to grow in size and triggered an increase in the surface area of intestinal cells that absorb nutrients. “These findings demonstrate that gut microbes enable mammals to harvest more energy from food as a way to adapt to the increased energy demand associated with long periods of cold exposure, thereby helping to protect against hypothermia,” Trajkovski says. “We were surprised to see that gut microbes had such dramatic effects on the structure and function of the intestine.”
Moving forward, the researchers plan to study the molecular mechanisms by which gut microbes sense changes in the environment to affect the energy balance of the host. Another avenue of investigation centers on the idea that certain bacteria may prevent obesity by remodeling intestinal tissue and thereby decreasing the absorption of nutrients in the gut.
Public Release: 8-Dec-2015
Living longer and healthier in mind but not in body
Newcastle University
Women are now spending fewer years with cognitive impairment but more years with disability compared to 20 years ago, new research has revealed.
Experts have shown that between 1991 and 2011 women’s life expectancy at age 65 increased by 3.6 years but they identified that the female body doesn’t age as well as its mind.
A study by Newcastle University, UK, and the University of Cambridge, UK, published in The Lancet, has revealed that women lived approximately 2.5 months less with moderate or severe cognitive impairment and six months fewer with mild cognitive impairment, such as problems with memory and thinking.
However, this is balanced by the fact that at age 65 females now spend around seven months more with moderate or severe disability and 2.5 years more with mild disability.
Meanwhile, overall men’s life expectancy increased by 4.5 years but they had only 1.3 years more with mild disability and there was no increase in the years spent with moderate or severe disability, or mild or worse cognitive impairment.
Professor Carol Jagger, from Newcastle University’s Institute for Ageing, led the analysis of the research.
She said: “The big unanswered question is whether our extra years of life are healthy ones and the aim of our research was to investigate how health expectancies at age 65 years and over changed between 1991 and 2011.
“One possibility for the increased years women are living with mild disability might be the rise in obesity levels over the decades, but there may also be particular conditions, or just more multiple diseases, which are a feature of very old age.”
The research team compared two rounds of the Cognitive Function and Ageing Study, done in England in 1991 and 2011.
Health expectancy was measured in three ways: self-perceived health, life without disability, and time free from cognitive impairment. For the study a total of 7,635 people aged 65 and over were analysed in Newcastle, Cambridge and Nottingham.
Analysis of the Health Survey for England for those aged 65+ over a similar time period showed problems with vision and hearing did not account for increases in disability.
Nevertheless, stability in self-care activities, like cooking, and increases in mobility limitations, such as walking 200 yards and climbing stairs, may contribute to gains in mild disability.
Professor Carol Brayne, from the University of Cambridge, was overall lead for the study.
She said: “The findings suggest a compression of cognitive morbidity when comparing older people now compared to 20 years ago in England. This is very good news and consistent with our earlier reporting of a reduction in age specific prevalence of dementia across two decades.”
Health expectancies are important indicators to monitor population health trends and inequalities internationally, nationally and regionally.
It is necessary for Government to get a clear indication if people are living longer, healthier lives as it can have an impact on the economy, housing and employment opportunities.
Future work will examine the reasons for the increase in years with disability. The researchers will look at which diseases and conditions are responsible for the rise in mild disability and whether patterns prevail across all the regions studied.
Professor Jagger added: “Our findings have important implications for Government, employees and individuals with respect to raising the state pension age and extending working life.
“It is also necessary for community care services and family carers who predominantly support those with mild to moderate disability to enable them to continue living independently.”
In most developed countries worldwide life expectancy is increasing at the rate of at least two years every decade, and, for life expectancy at age 60, shows no sign of slowing down.
Newcastle University’s Institute for Ageing held a conference today (Tuesday, December 8), which focused on ‘The economic and social impact of ageing’ – Professor Jagger opened the event.
Public Release: 8-Dec-2015
Alcohol aromatherapy eases nausea in the ER
American College of Emergency Physicians
WASHINGTON — Nauseated patients in the emergency department who sniffed pads saturated with isopropyl alcohol were twice as likely to obtain relief from their symptoms as nauseated patients who sniffed pads saturated with saline solution, according to a study published online today in Annals of Emergency Medicine (“Isopropyl Alcohol Nasal Inhalation for Nausea in the Emergency Department: A Randomized Controlled Trial”).
“We love it when we find a cheap, easy and fast way to bring relief to our patients,” said lead study author Kenneth Beadle, EMPA-C, of the San Antonio Uniformed Services Health Education Consortium in San Antonio, Texas. “Nausea and vomiting are the chief complaint for nearly five million emergency patients every year, so this remedy has the potential to help a lot of people.”
Researchers administered pads saturated with either isopropyl alcohol or saline solution and instructed nauseated patients to inhale deeply through their noses from the pad every two minutes for four minutes, for a maximum of three inhalations. Within 10 minutes of the intervention, the nausea score in the alcohol patients was half that of the saline solution patients. The satisfaction score for the alcohol patients was double the satisfaction score for the saline solution patients.
“Alcohol wipes are safe and there were no adverse effects,” said Dr. Beadle. “Further research is warranted to test the duration of the effect and performance in comparison to traditional, pharmaceutical anti-emetics. That said, the available evidence suggests these alcohol wipes may be a potent tool for relieving nausea and improving satisfaction among our emergency patients.”
Public Release: 7-Dec-2015
Migraine triggers may all act through a common pathway
Wiley
Migraines can be triggered by a variety of factors, including stress, sleep disruption, noise, odors, and diet. The findings of a new Headache review indicate that many of these factors converge on a common pathway involving oxidative stress.
When Dr. Jonathan Borkum at the University of Maine examined studies on migraine triggers published between 1990 and 2014, he found that nearly all traditional triggers had a propensity to generate oxidative stress, an imbalance between the production of free radicals and the ability of the body to counteract their harmful effects. The findings suggest that antioxidants might help prevent or preempt migraines.
“These data hint that an acute migraine attack may be an attempt by the brain to protect itself, and possibly–when you look at certain chemicals released during an attack–to heal itself,” said Dr. Borkum. “Understanding migraines may ultimately teach us how we, too, can protect the brain.”
Plant compound found in spices and herbs increases brain connections
Brazilian research shows that the flavonoid apigenin has potential to treat diseases like schizophrenia, depression, Alzheimer’s and Parkinson’s
D’Or Institute for Research and Education
Brazilian researchers from D’Or Institute for Research and Education (IDOR), Federal University of Rio de Janeiro (UFRJ) and Federal University of Bahia (UFBA) have demonstrated in laboratory that apigenin, a substance found in parsley, thyme, chamomile and red pepper, improves neuron formation and strengthens the connections between brain cells.
Previous experiments with animals had already shown that substances from the same chemical group as the apigenin, known as flavonoids, positively affect memory and learning. Many studies highlight the potential of flavonoids to preserve and enhance brain function. While the effectiveness of flavonoids for brain health is not an entirely new concept, this research is the first to show the positive effects of apigegin directly on human cells and the first to unraveling its mechanism.
The scientists observed that just by applying apigenin to human stem cells in a dish they become neurons after 25 days – an effect they would not see without the substance. Moreover, the neurons that were formed made stronger and sophisticated connections among themselves after being treated with this natural compound.
“Strong connections between neurons are crucial for good brain function, memory consolidation and learning”, says neuroscientist from IDOR and UFRJ Stevens Rehen, leader author of the paper published today at Advances in Regenerative Biology.
The research team conducted by Rehen demonstrated that apigenin works by binding to estrogen receptors, which affect the development, maturation, function, and plasticity of the nervous system. This group of hormones is known to delay the onset of psychiatric and neurodegenerative disorders such as schizophrenia, depression, Alzheimer’s and Parkinson’s disease. However, the use of estrogen-based therapies is limited by the increased risk of estrogen-dependent tumors and cardiovascular problems.
Researchers believe apigenin can be used as an alternative approach on future treatments for neurodegenerative diseases as well as in neuronal differentiation strategies in laboratory.
“We show a new path for new studies with this substance”, points out Rehen. “Moreover, flavonoids are present at high amounts in some foods and we can speculate that a diet rich in flavonoids may influence the formation of neurons and the way they communicate within the brain.”