Tag Archives: Medical school

Foe Turns Friend

A-beta, a protein implicated in Alzheimer’s, may be the brain’s shield against germs.
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For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of.

The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognising friends and family.

But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defences against invading bacteria and other microbes.

Other Alzheimer’s researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing.

The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease.

To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.

That evening, Tanzi wandered into the office of a junior faculty member, Robert Moir, and mentioned what he had seen. As Tanzi recalled, Moir turned to him and said, “Yeah, well, look at this.”

He handed Tanzi a spreadsheet. It was a comparison of A-beta and a well-known protein of the innate immune system, LL-37. The likenesses were uncanny. Among other things, the two proteins had similar structures. And like A-beta, LL-37 tends to clump into hard little balls.

In rodents, the protein that corresponds to LL-37 protects against brain infections. People who make low levels of LL-37 are at increased risk of serious infections and have higher levels of atherosclerotic plaques, arterial growths that impede blood flow.

The scientists could hardly wait to see if A-beta, like LL-37, killed microbes. They mixed A-beta with microbes that LL-37 is known to kill — listeria, staphylococcus, pseudomonas. It killed eight out of 12. “We did the assays exactly as they have been done for years,” Tanzi said. “And A-beta was as potent or, in some cases, more potent than LL-37.”

Then the investigators exposed the yeast Candida albicans, a major cause of meningitis, to tissue from the hippocampal regions of brains from people who had died of Alzheimer’s and from people of the same age who did not have dementia when they died.

Brain samples from Alzheimer’s patients were 24 per cent more active in killing the bacteria. But if the samples were first treated with an antibody that blocked A-beta, they were no better than brain tissue from non-demented people in killing the yeast.

The innate immune system is also set in motion by traumatic brain injuries and strokes and by atherosclerosis that causes reduced blood flow to the brain, Tanzi noted.

And the system is spurred by inflammation. It’s known that patients with Alzheimer’s have inflamed brains, but it hasn’t been clear whether A-beta accumulation was a cause or an effect of the inflammation. Perhaps, Tanzi said, A-beta levels rise as a result of the innate immune system’s response to inflammation; it may be a way the brain responds to a perceived infection. But does that mean Alzheimer’s disease is caused by an overly exuberant brain response to an infection?

That’s one possible reason, along with responses to injuries and inflammation and the effects of genes that cause A-beta levels to be higher than normal, Tanzi said. However, some researchers say that all the pieces of the A-beta innate immune systems hypothesis are not in place.

Dr Norman Relkin, director of the memory disorders programme at New York-Presbyterian / Weill Cornell hospital, said that although the idea was “unquestionably fascinating”, the evidence for it was “a bit tenuous”.

As for the link with infections, Dr Steven DeKosky, an Alzheimer’s researcher at the Virginia School of Medicine, noted that scientists have long looked for evidence linking infections to Alzheimer’s and have come up mostly empty handed.

But if Tanzi is correct about A-beta being part of the innate immune system, that would raise questions about the search for treatments to eliminate the protein from the brain.

“It means you don’t want to hit A-beta with a sledgehammer,” Tanzi said.

But other scientists not connected with the discovery said they were impressed by the new findings. “It changes our thinking about Alzheimer’s disease,” said Dr Eliezer Masliah, who heads the experimental neuropathology laboratory at the University of California, San Diego.

Source : New York Times News Service

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Air Pollution May Cause Appendicitis

Air pollution is already linked to respiratory and cardiovascular ills, and now researchers say the dirty air you breathe may also cause appendicitis.

Authors of a new study published in the Oct. 5 issue of the Canadian Medical Association Journal found that cases of appendicitis go up when the air is dirtier.

“This makes us think about the underlying cause of appendicitis that could potentially be linked to air pollution,” said Dr. Gilaad G. Kaplan, senior author of the study and assistant professor of medicine in the division of gastroenterology at the University of Calgary in Alberta. “Air pollution is a modifiable risk factor. If these findings are confirmed and we are able to legislate better air pollution control, cleaner air, then potentially we could prevent more cases of appendicitis.”
But at this early point in the research, the implications are not so clear-cut, warned another expert.

“It’s provocative, but there’s a huge difference between correlating any number of factors with a disease and proving that any of these factors might actually cause a disease, and this study fails to show causation,” said Dr. F. Paul Buckley III, assistant professor of surgery at the Texas A&M Health Science Center College of Medicine and a surgeon at Scott & White Healthcare Round Rock, Texas.

“Do we all want to decrease pollution? Yes. Is that going to decrease the incidence of appendicitis? I doubt it,” said Buckley.

Parts of the findings were presented at a conference a year ago.

No one really knows why appendicitis, or swelling and infection of the appendix, occurs.

Appendicitis cases rose significantly in the late 19th century and early 20th century, as industrialization took hold. Cases declined in the middle and later parts of the last century, at about the time clean air legislation gained headway. Meanwhile, countries that are just now industrializing have increasing rates of the condition, the study authors stated.

A prevailing theory is that appendicitis occurs when the opening to the appendix, a pouch-like organ attached to the large intestine, gets blocked. Specifically, some experts believe that lower fiber intake among citizens of industrialized countries leads to obstruction of the appendix by the stool.

But that doesn’t explain the decreased incidence of appendicitis in the second half of the 20th century, Kaplan said.

Air pollution is already linked with a wide range of health conditions, most notably respiratory diseases and cardiovascular disease, including heart attack and stroke.

Kaplan and his colleagues looked at more than 5,000 adults who were hospitalized in Calgary with appendicitis between April 1, 1999, and the end of 2006. This data was cross-referenced with an analysis of air pollutants the week prior to the admissions.

“We found that individuals were more likely to come in with appendicitis in weeks with higher concentrations of air pollutants, specifically ozone and nitrogen dioxide,” Kaplan said.

More appendicitis admissions took place during Canada’s warmest months (April through September, when people are more likely to be outdoors), and men seemed more likely to be affected by air pollutants than women. It’s unclear why this gender difference exists, the researchers said.

Kaplan theorizes that inflammation may explain the link — if it proves to exist — between air quality and appendicitis.

“It’s speculative, but air pollution might be driving inflammation which triggers appendicitis,” he said. “We’re a few steps away before we can make that statement. We need to confirm and replicate these findings.”

Kaplan and his co-authors plan more studies in multiple cities in Canada.

Last year, Forbes magazine rated Calgary as the world’s cleanest city and Baku, Azerbaijan, as the dirtiest.

Source: Health News. 5Th.Oct.’09

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Do Some Fish Oil Supplements Contain Mercury?

Fish oil supplements are increasingly popular, but it has sometimes been suggested that they could also expose you to the harmful pollutants found in some species of fish.
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However, studies have found that most of the widely available supplements contain little or no mercury, dioxins or PCBs.

Most companies use species of fish that are lower on the food chain, like cod and sardines, that accumulate less mercury. Many companies also distill their oils to help remove contaminants.

A report by ConsumerLab.com, which conducts independent tests of supplements, examined 41 common fish oil products and found none contaminated with mercury or PCBs. Another report, by researchers at Harvard Medical School and at Massachusetts General Hospital, studied five popular brands of fish oil and found that the brands had “negligible amounts of mercury.”

Resources:
New York Times March 23, 2009
Archives of Pathology and Laboratory Medicine Dec 2003;127(12):1603-5 (Free Full Text Article)

Hot Chillies Can Help Mitigate Pain

Capsaicin, the active agent in spicy hot chili peppers, often acts as an irritant, but it may also be used to reduce pain.

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Feng Qin, associate professor of physiology and biophysics at the University at Buffalo School of Medicine, and Jing Yao used capsaicin to unravel how pain-receptor systems can adapt to painful stimuli.

For example, adaptation happens when your eyes adjust from a dark movie theatre during a matinee to the bright sunlight outside. Whether pain receptors truly adapt or rescale their responses (versus simply desensitising) has been an open question.

Scientists had previously linked the analgesic or pain-relieving effects of capsaicin to a lipid called PIP2, found in cell membranes. When capsaicin is applied to the skin it induces a strong depletion of PIP2 in the cell membrane.

“The receptor acts like a gate to the neurons,” said Qin. “When stimulated it opens, letting outside calcium enter the cells until the receptor shuts down, a process called desensitisation.”

“The analgesic action of capsaicin is believed to involve this desensitization process. However, how the entry of calcium leads to the loss of sensitivity of the neurons was not clear,” he said, according to a Buffalo release.

Capsaicin creams are commonly sold over the counter as effective treatment for a variety of pain syndromes, from minor muscle or joint aches to those that are very difficult to treat, such as arthritis and neuropathic pain.

Sources:The Times Of India

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Anger Alert for Heart

Episodes of anger may lead to potentially lethal abnormal heart rhythms in patients with heart disease and those who are survivors of heart attacks, a medical study has suggested.

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The study by researchers at the Yale University School of Medicine in the US is the first to show how emotion triggers a distinct pattern of electrical activity that contributes to arrhythmias — abnormal heart rhythms.

The researchers who monitored a group of 62 patients found that those with high levels of anger-induced electrical cardiac activity called T-wave alternans were more likely to experience arrhythmias than patients with low levels of this electrical activity.

Anger appeared to increase the risk of arrythmias by up to 10 times. The findings will appear shortly in the Journal of the American College of Cardiology.

“Our study identified individuals vulnerable to increased electrical instability due to emotion,” said Rachel Lampert, associate professor of medicine at Yale who has been exploring how mental stress can disturb heart rhythms.

The researchers studied patients with heart problems who had implantable cardioverter-defibrillators — small, battery-powered devices in the chest from where they constantly monitor the heart rate and rhythm.

When the device detects abnormal heart rhythms, it delivers an electrical shock to the heart muscle to stop the arrhythmia and return the heart to its normal rhythm.

The study examined incidence of arrhythmias over three years and found that patients with arrhythmias had higher T-wave alternans induced by anger than patients who had not experienced arrhythmias.

Arrhythmias of concern are rare in healthy people. “The implications of our findings are for the increasing number of people who have survived a heart attack or are living with heart failure,” Lampert told The Telegraph.

Cardiologists believe it is important to identify patients who are at risk of developing life-threatening arrhythmias. The results suggest that therapy to help patients deal with anger and other negative emotions may reduce arrhythmias, said Lampert.

Sources:
The Telegraph (Kolkata, India)

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