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Archive for February, 2015

A newly characterized group of pharmacological compounds block both the inflammation and nerve cell damage seen in mouse models of multiple sclerosis, according to a study conducted at the Icahn School of Medicine at Mount Sinai and published online this week in the journal Nature Neuroscience.

Multiple sclerosis is a disease of the brain and spinal cord, where for unknown reasons, the body’s immune system begins an inflammatory attack against myelin, the protective coating that surrounds nerve fibers. Once myelin is stripped from these fibers, the become highly susceptible to damage, which is believed to underlie their destruction, leading to the steady clinical decline seen in progressive forms of .

“The compounds identified in this study, when administered orally, both reduced the inflammation that is a hallmark of multiple sclerosis and protected against the seen in mouse models of the disease,” said Jeffery Haines, PhD, a post-doctoral fellow at Mount Sinai and the study’s lead author. “The multiple sclerosis drugs currently on the market and being tested elsewhere seek to reduce the immune attack on cells, but none target neurodegeneration nor do they work to restore . The findings of this new study represent an exciting step in the process of advancing new oral treatment options.”

Previous research conducted at Mount Sinai found that the trafficking of protein molecules between the nucleus (the cellular compartment containing the genetic information of the cell) and the cytoplasm is altered in neurodegenerative disease. The molecule that shuttles proteins between the nucleus and cytoplasm, XPO1 (also called CRM1,) has been implicated in multiple sclerosis and a number of other diseases.

Specifically, the Mount Sinai study was designed to test whether pharmacological compounds designed to block the function of XPO1/CRM1 could stop disease progression in mouse models that exhibit some of the characteristics of MS. Researchers found that two chemical agents (called KPT-276 and KPT-350) prevented XPO1/CRM1 from shuttling cargo out of the nucleus of nerve cells, which protected them from free radicals and structural damage. The compounds also stopped inflammatory cells from multiplying, thereby reducing inflammation.

Mice showing hindlimb paralysis were able to regain motor function within two weeks after KPT-276 or KPT-350 were orally administered.

“The study results elucidate the molecular mechanisms underlying disease progression in multiple sclerosis models, providing a basis for future clinical trials to determine safety and efficacy of these chemical agents in humans with demyelinating disorders,” says Patrizia Casaccia, MD, PhD, Professor of Neuroscience, Genetics and Genomic Sciences at Mount Sinai and senior author of the study.

Because traffic of molecules between the nucleus and the cytoplasm of nerve cells is altered in several other neurodegenerative disorders, targeting nuclear transport may have broader therapeutic implications in diseases like (ALS) and Alzheimer’s disease.

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A new study by a UT Dallas researcher challenges a long-accepted scientific theory about the role the hippocampus plays in our unconscious memory.

For decades, scientists have theorized that this part of the brain is not involved in processing unconscious memory, the type that allows us to do things like button a shirt without having to think about it.

But research by Dr. Richard Addante, a senior lecturer in the School of Behavioral and Brain Sciences, raises doubts about that theory.

“These intriguing new findings raise important questions regarding the organization of memory systems and will doubtlessly receive a great deal of attention from other investigators,” said Dr. Bert Moore, dean of the School of Behavioral and Brain Sciences and Aage and Margareta Møller Distinguished Professor. “Dr. Addante’s careful, thoughtful work provides exciting insights into the brain bases of memory.”

Addante used electroencephalography (EEG) to test brain wave patterns while giving memory tests to amnesia patients with damaged hippocampi. He then compared those results with control subjects as part of the study, which was published recently in the journal NeuroImage.

Much of the knowledge about the hippocampus and how our brains organize memory comes from research at the Massachusetts Institute of Technology on an amnesia patient known in textbooks as “Patient H.M.” The patient was later revealed to be Henry Molaison, who died in 2008.

Molaison’s hippocampus and other tissue were removed in 1957 to treat intractable epilepsy. The surgery was effective in reducing the seizures, but researchers were surprised to find that Molaison could no longer form new long-term memories, though he could recall his past before the surgery and could also exhibit preserved unconscious memory abilities.

Given the research on Molaison, Addante expected the amnesia patients to perform well on the unconscious memory tests when he began his study. If the hippocampus is not needed for unconscious memory, they should perform just as well as the control subjects, he believed.

hippocampus-unconscious-memory-system-public

The researcher used electroencephalography (EEG) to test brain wave patterns while giving memory tests to amnesia patients with damaged hippocampi. This image is for illustrative purposes only.

But the patients’ EEGs showed much different results than the others, forcing Addante to change his hypothesis.

Challenging an established scientific theory — widely published in major neuroscience textbooks — was a long shot, he said. Addante wrestled with whether the huge undertaking was worth the investment.

“I didn’t know if the research would ever see the light of day,” said Addante, who was a graduate researcher at the University of California, Davis when he tested the patients. “But I was committed to solving a puzzle and have never quit anything thus far in life.”

Now that the work is published, Addante hopes the research will lead to more studies in this area. He said there’s a need for more research using EEG to study unconscious memory.

“If nothing else, prove it wrong,” Addante said. “If that happens, that’s awesome, too, because that’s science and progress.”

About this memory research

Contact: Kim Horner – UT Dallas
Source: UT Dallas press release
Image Source: The image is credited to Camillo Golgi and is in the public domain
Original Research: Abstract for “A critical role of the human hippocampus in an electrophysiological measure of implicit memory” by Richard James Addante inNeuroImage. Published online January 4 2015 doi:10.1016/j.neuroimage.2014.12.069

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Why 10 P.M. Is The Perfect Bedtime

Here’s why you should consider going to bed before midnight.

I’m going to take a wild guess that you already know that sleep affects how well you function. You’re also probably aware that sleep quality is part of the equation (not just quantity).

But the truth is, the time you go to bed, what you do in the hours before going to bed, and what you do when you wake up ALL have a big impact on your rest, according to wellness expert Shawn Stevenson. Shawn has studied the optimal methods for maximizing the quality of your sleep, and has looked at how everything from the set-up of your bedroom to how much water you drink during the day can affect your ZZs.

And considering Shawn’s wealth of knowledge on sleep, it stands to reason that he knows a thing or two about bedtimes. I asked Shawn if there is a golden bedtime for everyone, and his response was two-fold: One, everyone’s body IS different, so it’s most important to listen to what works best for you. But if you haven’t tried going to bed before midnight, give it a chance. We are biological beings affected by the sun’s patterns, so if we go to bed with the sun and wake up with it, we’re working with our natural circadian rhythm. In fact, the closer we can get to the sun’s patterns, the better our energy is. He recommends a 10 p.m. to 6 a.m. sleep schedule (noting that it’s OK to be a little flexible with those times). Give it a try.

He offered some other tips for setting yourself up for a good night’s rest:

  • Stop looking at electronic device screens two hours before you want to fall asleep. (If that’s not going to happen, you can get some cool shades to block the blue light that keeps you up.)
  • Work out early in the day (even if it’s just a 10-minute set of ab exercises when you wake up).
  • Pay attention to what you’re eating in the second half of the day: Avoid caffeine, sugar, and dairy.

If you change your sleep habits (one at a time if need be), you’ll start to see changes in your sleep quality quickly. Better sleep creates better energy to carry you through your day. And who doesn’t need more of that?

Want to know more of Shawn’s tips for optimizing your daily habits and routines? You can listen to my full interview with him here.

For more information and links to the resources Shawn recommends, click here.

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stephen-hawking

Stephen Hawking has a long list of warnings about threats to humanity.

Stephen Hawking may be most famous for his work on black holes and gravitational singularities, but the world-renowned physicist has also become known for his outspoken ideas about things that could destroy human civilization.

Hawking suffers from a motor neuron disease similar to amyotrophic lateral sclerosis, or ALS, which left him paralyzed and unable to speak without a voice synthesizer. But that hasn’t stopped the University of Cambridge professor from making proclamations about the wide range of dangers humanity faces — including ourselves.

Here are a few things Hawking has said could bring about the demise of human civilization. [End of the World? Top Doomsday Fears]

Artificial intelligence

Hawking is part of a small but growing group of scientists who have expressed concerns about “strong” artificial intelligence (AI) — intelligence that could equal or exceed that of a human.

“The development of full artificial intelligence could spell the end of the human race,” Hawking told the BBC in December 2014. The statement was in response to a question about a new AI voice-synthesizing system that Hawking has been using.

Hawking’s warnings echo those of billionaire entrepreneur Elon Musk, CEO of SpaceX and Tesla Motors, who has called AI humanity’s “biggest existential threat.” Last month, Hawking, Musk and dozens of other scientific bigwigs signed an open letterdescribing the risks, as well as the benefits, of AI.

“Because of the great potential of AI, it is important to research how to reap its benefits while avoiding potential pitfalls,” the scientists wrote in the letter, which was published online Jan. 11 by the Future of Life Institute, a volunteer organization that aims to mitigate existential threats to humanity.

But many AI researchers say humanity is nowhere near being able to develop strong AI.

“We are decades away from any technology we need to worry about,” Demis Hassabis, an artificial intelligence researcher at Google DeepMind, told reporters this week at a news conference about a new AI program he developed that can teach itself to play computer games. Still, “It’s good to start the conversation now,” he added.

Human aggression

If our machines don’t kill us, we might kill ourselves. Hawking now believes that human aggression might destroy civilization.

The physicist was giving a tour of the London Science Museum to Adaeze Uyanwah, a 24-year-old teacher from California who won a contest from VisitLondon.com. When Uyanwah asked, “What human shortcomings would you most like to alter?” Hawking responded:

“The human failing I would most like to correct is aggression. It may have had survival advantage in caveman days, to get more food, territory or partner with whom to reproduce, but now it threatens to destroy us all,” The Independent reported.

For example,a major nuclear war would likely end civilization, and could wipe out the human race, Hawking added. When asked which human quality he would most like to magnify, Hawking chose empathy, because “it brings us together in a peaceful, loving state.”

Hawking thinks space exploration will be important to ensuring the survival of humanity. “I believe that the long-term future of the human race must be space, and that it represents an important life insurance for our future survival, as it could prevent the disappearance of humanity by colonizing other planets,” Cambridge Newsreported.

Alien life

But Hawking had made ominous warnings even before these recent ones. Back in 2010, Hawking said that, if intelligent alien life exists, itmay not be that friendly toward humans.

“If aliens ever visit us, I think the outcome would be much as when Christopher Columbus first landed in America, which didn’t turn out very well for the Native Americans,” Hawking said during an episode of “Into the Universe with Stephen Hawking,” a show hosted by the Discovery Channel, reported The Times, a U.K.-based newspaper.

Advanced alien civilizations might become nomads, looking to conquer and colonize whatever planets they could reach, Hawking said. “If so, it makes sense for them to exploit each new planet for material to build more spaceships so they could move on. Who knows what the limits would be?”

From the threat of nefarious AI, to advanced aliens, to hostile humans, Hawking’s outlook for humanity is looking pretty grim.

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http://screen.yahoo.com/10-things-youll-surprised-dog-151918540.html

‘warning’ – pop-ups

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At Martin O’Riordan’s cardiology practice in the Philadelphia area, it happens weekly.

A 45- or 50-year-old patient mentions that her father had a heart attack at the same age. Worried that the same fate will befall her despite being in good health, she takes baby aspirin every day.
O’Riordan’s typical response: Please stop.
Physicians have known for decades that daily, low-dose aspirin makes sense for patients who have had a heart attack or stroke, as it sharply reduces the chance of having a second one.
But for people who have never had one of these cardiovascular “events,” the thinking on aspirin is less clear, despite two recent large-scale studies. The reason for caution is the very reason that aspirin wards off heart attacks and strokes: It interferes with blood clotting, putting the patient at higher risk of serious gastrointestinal bleeding.

“People have kind of looked at it as, ‘Aspirin, an apple, a glass of milk, it’s all good for you,’ ” said O’Riordan, who is on staff at Lankenau Medical Center. “Aspirin is a medication.”

It is a medication drawing renewed scrutiny, 30 years after the Food and Drug Administration approved its use after a heart attack.

Evidence suggests it is also a good idea for some people who have not had a heart attack but who are at risk of having one — those with multiple risk factors such as high cholesterol, high blood pressure or diabetes. But the FDA has not approved it for that use.

And no one is precisely sure at what point aspirin’s benefits outweigh the risk of bleeding, said Dr. J. Michael Gaziano, a researcher with the division aging at Brigham and Women’s Hospital in Boston.

“We know that it prevents heart attacks in everybody,” said Gaziano, who is helping to oversee one of three ongoing aspirin trials. “What we don’t know is exactly what’s the break point.”

One issue is deciding how much “weight” to assign to a serious bleed. It is generally not as bad as a heart attack, yet some aspirin-related bleeding is severe enough to require a blood transfusion.

Another problem is the low rate of heart attacks in the broader population, which is dropping with healthier lifestyles. Statistically, it is hard to measure a reduction in something that is uncommon to begin with.

Among those who have never had a heart attack or stroke, studies have linked aspirin use with a nearly 12 percent reduction in the chance of suffering one. But that is a reduction in a very small number. Instead of 57 heart attacks and strokes per year in a group of 10,000 people, you get 51, according to a meta-analysis published in the Lancet.

The impact on serious bleeding, meanwhile, varies from study to study. As with the drop in heart attacks, however, the yearly increase in major bleeds per 10,000 people is in the single digits — though higher in older people.

O’Riordan and other physicians use one of several “risk calculators” to determine a patient’s chance of a cardiovascular event in the next 10 years, generally recommending aspirin if that risk is above 6 to 10 percent.

Researchers have found that some of these calculators, popular online, may overestimate the chance of a heart attack. The most recent evidence was published recently in the Annals of Internal Medicine.

Still, the numbers are compelling enough for Cherry Hill, Pennsylvania, resident Frank Plunkett, who has not had a heart attack but who has taken daily aspirin for more than a decade.

Plunkett has high blood pressure and a total cholesterol count that at times has exceeded 200, so his physician told him aspirin was a good bet.

“I think it helps prevent clots and keeps my blood vessels from getting clogged,” said Plunkett, chair of the school of criminal justice at the ITT Technical Institute in Levittown, Pennsylvania.

The FDA has taken a more cautious stance. In May, the agency rejected Bayer HealthCare’s request to market low-dose aspirin for use by people who have not had a heart attack.

Yet many people take it — even those who are at low risk of heart disease, according to a January study in the Journal of the American College of Cardiology.

In a population of nearly 69,000 patients at 119 cardiology practices, study authors found 11.6 percent were taking aspirin despite having less than a 6 percent risk of cardiovascular disease in 10 years.

That number reflected only those for whom aspirin use was recorded in the physician’s chart. So the rate of people taking aspirin inappropriately may actually have been higher, said lead author Ravi S. Hira, an interventional cardiology fellow at Baylor College of Medicine in Houston.

Though the “worried well” sometimes take aspirin when they should not, studies have found some heart attack victims fail to take it even though they should, said Dr. Garret FitzGerald, a professor at the University of Pennsylvania’s Perelman School of Medicine.

“That’s the human condition, right?” FitzGerald said.

The first clues that aspirin could prevent heart attacks came in the late 1940s, when California physician Lawrence Craven noticed patients who had their tonsils removed were prone to bleeding if they took aspirin for the pain.

He hypothesized the medicine might interfere with the formation of clots that can lead to heart attacks, and science eventually proved him right.

In the 1980s, FitzGerald and his Penn colleagues conducted some of the key research leading to a consensus that even a low dose of the drug could prevent a second heart attack.

More recent research suggests aspirin may have another benefit. Studies have associated it with a reduced rate of colon cancer, though FitzGerald called that “an interesting suggestion rather than compelling evidence.”

But make no mistake — that longtime staple of medicine cabinets is a drug. Use it with caution.

Bottom line: Aspirin is more potent than many people realize, said O’Riordan, of Mercy Health System.

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NEVER go off your meds without discussing it with your doctor;
TALK to your doctor before trying any of the following!
By ; WebMD Health News; Reviewed by Brunilda Nazario, MD

Feb. 27, 2015 — There may be hope for hard-to-treat depression as scientists explore novel ways to help people who have the often crippling condition.

Recently, a number of studies have suggested the benefits of Botox, ketamine, and certain sometimes-unexpected means of treating depression.

“I’m excited in general, and I’m curious,” says Peter D. Kramer, MD, author of Listening to Prozac and Against Depression.

Each year, around 16 million U.S. adults battle major depression. Many of them benefit from antidepressants. But as many as a third get depressive symptoms despite medication. And side effects, which can include weight gain, nausea, and insomnia, are troublesome for some patients. That leaves many people with depression searching for alternatives.

But if Kramer is hopeful about the newer, novel ways to treat the condition, he’s also cautious. The studies backing those treatments aren’t conclusive, and none of the approaches have been approved by the FDA to treat depression (though some, such as ketamine, have been approved for other uses).

“Things are merely hopeful until they are demonstrated [safe and effective],” Kramer says. “It’s always hard to tell what’s going on, but it’s a very interesting time, and I think some of them will come through.”

Here’s a closer look at what might be used to help treat depression in years to come.

Ketamine. Already in use in certain clinics and in some emergency departments around the country, ketamine is an anesthetic most often used during surgery. It’s given through an IV, and it quickly easessymptoms of depression, often in a matter of hours. The benefit is temporary, though.

One recent study found it to be very good at helping curb suicidalthoughts in severely depressed people. But it’s expensive, still experimental as a depression treatment, and can cause hallucinations and other side effects.

“Some people are very uncomfortable with the side effects,” says Alan Manevitz, MD, a psychiatrist who specializes in treatment-resistant depression at Lenox Hill Hospital in New York City.

Nitrous oxide, or laughing gas. This is an anesthetic commonly used by dentists. A small study published last December reports that nitrous oxide improved depression symptoms within less than 2.5 hours.

Unlike ketamine, though, nitrous oxide had few side effects. The benefits lasted from 24 hours to a full week in some of the 10 people in the study. Much more research needs to be done on the safety and effectiveness of nitrous oxide, but Manevitz says it’s promising.

“For people who are in suicidal despair or crisis, it may, like ketamine, temporarily relieve that person and act as a bridge until other treatments start working,” he says.

Botox. Best known for temporarily erasing frown lines and crow’s feet, onabotulinumtoxinA (Botox) has recently attracted interest as a novel means of lifting major depression. The theory is simple: If you can’t frown, you won’t be sad. And some research has borne this out.

A single Botox injection into the facial “frown muscles” provided lasting relief from depression symptoms, according to a study published last spring in the Journal of Psychiatric Research. Another study found similar effects following Botox injections into frown lines around the eyebrows. Many questions remain, though.

“The Botox is very interesting, and the best evidence [it helps] is as an add-on to antidepressants, but what’s going on?” asks Kramer. “Is it really feedback to the brain, that if you can’t frown, do you feel more resilient? Or is it that people respond to you differently?”

Anti-inflammatory medications. Inflammation has been linked to depression for several years now, says Brown. A recent review of studies, published in JAMA Psychiatry, further backs up the connection. The researchers found that painkillers such as celecoxib, ibuprofen, andnaproxen reduced depression symptoms. Another class of anti-inflammatory drugs, called cytokine inhibitors, also showed some benefit.

The authors of the review call their findings “proof of concept,” meaning that their results are strong enough to encourage further research. Another recent study reports that omega-3 fatty acids, which have anti-inflammatory properties, helped treat depression linked to chronic hepatitis C.

“If you could actually treat depression symptoms along these lines, that would be interesting,” Kramer says. “Some of the antidepressants are also anti-inflammatories, and some people have thought that maybe it’s just coincidence that they work on [the brain chemicals] serotonin and norepinephrine, and that the real effect is anti-inflammatory.”

Uncertain Future

The treatments listed above aren’t the only ones being tested.

Nasal sprays that have protein peptides or small molecules have shown some promise, Kramer and Manevitz say. A method called transcranial direct current stimulation, which uses electricity to change brain activity, is also being tested.

Mindfulness meditation is another promising addition to depression treatment, and exercise is known to help relieve symptoms, too.

If some of the newer treatments seem far-fetched, Manevitz points out that the same was said just a few years ago about transcranial magnetic stimulation (TMS), a non-invasive therapy that uses magnets to affect parts of the brain linked to mood.

“People looked at me cross-eyed and thought it sounded wacky,” he says. “Now, it’s an FDA-approved treatment for depression, and it’s used around the world.”

Which, if any, of these treatments prove effective is anybody’s guess at this point. Researchers have a lot of work ahead of them before any make it to patients in the clinic.

“So many medicines get lost in the pipeline,” Kramer says. “Either it’s hard to engineer them in ways that are not going to harm the kidneys or the liver, or the actual principle under which they are working turns out not to be right. It’s hard to give your heart to any one of them because they tend to disappoint.”

There was a LISTEN ‘pop-up’ HERE

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