POTENTIAL THERAPY FOR THE SUDAN STRAIN OF EBOLA COULD HELP CONTAIN SOME FUTURE OUTBREAK

From the FMS Global News Desk of Jeanne Hambleton August 27 2014   American Chemical Society ACS Chemical Biology

Scientists report a new potential weapon in the fight against a strain of ebola (above) that is just as deadly as the one currently devastating West Africa.

Ebola is a rare, but deadly disease that exists as five strains, none of which have approved therapies. One of the most lethal strains is the Sudan ebolavirus (SUDV). Although not the strain currently devastating West Africa, SUDV has caused widespread illness, even as recently as 2012.

In a new study appearing in the journal ACS Chemical Biology, researchers now report a possible therapy that could someday help treat patients infected with SUDV.

John Dye, Sachdev Sidhu, Jonathan Lai and colleagues explain that about 50-90 percent of ebola patients die after experiencing the typical symptoms of the disease, which include fever, muscle aches, vomiting and bleeding. Of the five known ebolaviruses, the Zaire (EBOV) and SUDV strains are the most deadly and cause the most recurring outbreaks.

Many studies have focused on EBOV, the culprit of the current epidemic, but much less attention has been placed on SUDV until now. To develop a therapy for SUDV, this research team turned to an antibody that Dye’s group previously reported.

The team’s antibody was directed against SUDV and was made in mice. But the human immune system could potentially recognize that antibody as foreign and ultimately get rid of it, preventing the antibody from treating the disease. To avoid this situation, they wanted to make a “humanized” version of the antibody.

In the newly published work, the team put the ebola-specific part of the mouse antibody onto a human antibody scaffold and made some changes to this molecule. They identified two versions that were able to fend off SUDV in laboratory tests on cells and in specially bred mice.

“These antibodies represent strong immunotherapeutic candidates for the treatment of SUDV infection,” say the researchers.

This research, however, is not expected to help with the current ebola outbreak that, as of mid-August, has killed at least 1,200 people. That is because antibodies that kill off one strain of the virus have not worked against other strains.

The U.S. Food and Drug Administration — which has not yet approved any ebola therapies — did allow two U.S. aid workers infected during the current outbreak to be treated with an experimental drug, which is a cocktail of antibodies specifically targeting EBOV.

NEW STUDY THROWS INTO QUESTION LONG-HELD BELIEF ABOUT DEPRESSION

From the FMS Global News Desk of Jeanne Hambleton 27 August 2014                                                  ACS Chemical Neuroscience American Chemical Society

New evidence puts into doubt the long-standing belief that a deficiency in serotonin — a chemical messenger in the brain — plays a central role in depression. In the journal ACS Chemical Neuroscience, scientists report that mice lacking the ability to make serotonin in their brains (and thus should have been “depressed” by conventional wisdom) did not show depression-like symptoms.

Donald Kuhn and colleagues at the John D. Dingell VA Medical Center and Wayne State University School of Medicine note that depression poses a major public health problem. More than 350 million people suffer from it, according to the World Health Organization, and it is the leading cause of disability across the globe.

In the late 1980s, the now well-known antidepressant Prozac was introduced. The drug works mainly by increasing the amounts of one substance in the brain — serotonin. So scientists came to believe that boosting levels of the signaling molecule was the key to solving depression. Based on this idea, many other drugs to treat the condition entered the picture. But now researchers know that 60 to 70 percent of these patients continue to feel depressed, even while taking the drugs. Kuhn’s team set out to study what role, if any, serotonin played in the condition.

To do this, they developed “knockout” mice that lacked the ability to produce serotonin in their brains. The scientists ran a battery of behavioral tests. Interestingly, the mice were compulsive and extremely aggressive, but did not show signs of depression-like symptoms. Another surprising finding is that when put under stress, the knockout mice behaved in the same way most of the normal mice did. Also, a subset of the knockout mice responded therapeutically to antidepressant medications in a similar manner to the normal mice. These findings further suggest that serotonin is not a major player in the condition, and different factors must be involved. These results could dramatically alter how the search for new antidepressants moves forward in the future, the researchers conclude.

The authors acknowledge funding from the Department of Veterans Affairs and the Department of Psychiatry and Behavioral Neurosciences at Wayne State University.

 

WHEN WILL I DIE? HOW I DECIDED WHETHER TO TEST FOR EARLY-ONSET ALZHEIMER’S

From the FMS Global News Desk of Jeanne Hambleton Aug. 19, 2014                                                     Stone Hearth Newsletter – Time Magazine By Matthew Thomas

 

People ask me all the time if I want to find out how and when I am going to die. But that is not exactly how they ask it. What they ask is whether I am going to get tested for the gene associated with early-onset Alzheimer’s disease. It is hard, though, to miss the subtext in the question: How morbidly curious are you? How much terror can you withstand?

I do not blame them. These friends know I am 39 and that my father started showing symptoms of Alzheimer’s in his early fifties (and possibly earlier). They know that after a handful of difficult years my father was diagnosed when I was a freshman in college and that he died less than a decade later. They wonder if I am going to take advantage of the remarkable opportunity science affords us to uncover our genetic destinies and plan accordingly.

Modern life is all about making us forget we are capable of dying. We love to feel in control of our mortality, even if we understand that that control is only an illusion. Alzheimer’s disease is the opposite of modern life. It is the ascendancy of entropy and chaos.

My father’s disease had a devastating effect on our family. It did not just take away our time with him and his with us. It also took away his time with the not yet conceived children who would populate the family in his absence. He would have been in his 70s now, surrounded by three grandchildren through my sister and two through my wife and me. It is painful to know what a resource he would have been for them and how much they have lost. He will live, faintly grasped, if at all, only in stories.

When he was still living, we tried to make the best of the situation. When my sister got married, my mother brought my father’s tux to the nursing home and had the staff dress him in it. After the ceremony, while everyone else headed to the reception, two limos carrying my immediate family took a detour to the nursing home for photos.

When I look at the framed shot of us huddled around my father in his wheelchair, I see how hard my sister is trying to keep her emotions in. She is smiling big, but tears are streaming down her face. We are all smiling hard, though there is no driving off the pain and awkwardness of the moment. Everyone’s looking at the camera except my father, who is gazing vacantly the other way, his mouth hanging open. Moments later we drove to the reception, leaving him behind, feeling terrible for doing so. I wanted him not to understand a thing that was happening in that scene, but you never knew what he knew.

For most of my youth, my father seemed to know everything. A universe of information swirled around in his brain. I could hardly put a question to him that he could not answer. The rare times he came up short, he pulled me into his study, took a book off the shelf, lay it on the desk and stood flipping through it with me. I think sometimes he pretended not to know things just so that we could look them up together.

Once, when I was about 10 and my sister about 14, we were walking with my father on the outskirts of his old neighborhood. He stopped in front of a town house and told us Winston Churchill’s mother was born there.

“The iconic English statesman of the century!” he said. “A mother from Brooklyn!” He gave us a look almost wild with the significance of what he was about to say. “The wit!” he said. “The chutzpah! That was the Brooklyn in him!”

Three decades later, I can still remember the moment, bathed in that ethereal light that we reserve for our happiest memories. Why do I remember it, though? How did such a quotidian moment burrow its way into my consciousness and survive? Was it the juxtaposition of incongruous worlds, England and Brooklyn? I don’t think so. I think it was the joy my father took in sharing his knowledge with us.

My father would have loved my twin children. They are 3 years old and full of vitality and personality. My son is unusually strong for such a skinny kid, and remarkably agile. He climbs whatever is available, with a monkey’s speed. When he sits at the piano and pounds the keys, it sounds as if he is playing a real song. My daughter is a sensitive cuddler who remembers everything.

“Daddy, is this from the hotel we stayed at?” she asked the other day, handing me a pad from a Marriott where we stayed six months ago.

Recently my daughter came into our bed in the early morning, lying between my wife and me, and started in on iguanas.

“Iguanas are baby alligators,” she said, and I chuckled at the powers of observation of a developing mind. “Can iguanas learn to open doors?” she asked, and after I offered the opinion that they could not, I pulled her close, gave her kisses and began to choke up.

Maybe when my twins are older, science will have caught up to this disease. We have the best scientific minds working on the problem of Alzheimer’s.

Much like the search for the cure for cancer, there is a massive payout at the end of the rainbow for anyone who comes up with a solution. If there is anything to put one’s faith in in the health care system, it is that the confluence of genius and capital will, in this case, produce the outcome if the outcome is producible. And I do believe it is producible. But if it is not produced in time, no amount of awareness of my fate, if it is to be my fate, is going to forestall its unfolding on me.

My wife and I have little battles over my forgetfulness. She asked me to fix the kink in the hose that runs from the humidifier in our basement to the French drain. A few days later, she gave up and fixed it herself. We had a grill delivered for our backyard, and the flame kept going out on it as soon as we lit it. I was supposed to call about it the next morning, but I would more or less forgotten that we had bought a grill in the first place when I heard my wife on the phone with the store. These are not terrifying signs in themselves — everyone is a little forgetful occasionally — but they make me pause enough to wonder if the worst is coming.

I am built like my father, I sound like him, and if I have a genetic mutation in one of three genes that are all variations of the apolipoprotein E gene, then I will likely develop early-onset Alzheimer’s like him. These genes are rare, accounting for only 1% to 5% of all Alzheimer’s cases. But if I inherited the mutation from my father, then I will probably get the disease.

My grandfather — my father’s father — died relatively young of other causes, so there’s no saying whether he would have gotten early-onset Alzheimer’s. No one else in the family had it that we know of. I have as good a chance of getting familial Alzheimer’s as I have of avoiding it. Genetic testing would settle the question for good.

But what would I gain by knowing I was getting Alzheimer’s? I would not gain another day with my family. I would not gain a leg up on planning. My wife and I have taken care of practical considerations. We have wills. My wife has a durable power of attorney that enables her to make decisions on my behalf. Every policy, every asset, is in both our names. We opened college savings accounts for the kids. I am working hard on my next book. How much more could I prepare?

After some deliberation, I have decided not to get genetic testing done. Instead, I am going to try to live every day as if I know that I am dying. The fact is, we are all dying. If I try to wring the most I can out of every moment, if I set aside time every day that my wife and I keep as inviolate as possible, if I give my wife and children quality interactions whenever we are in the same room, if I leave the smartphone on the counter and realize there is no information more important than the information I get in my interactions with my loved ones, then how different is any of that from what I would do if I knew I was getting Alzheimer’s?

Scientific studies suggest that my children are at just the age when they can begin to form lasting memories of their experiences. If I am aware that I am going to be gone someday and I consider it possible that that day will come far sooner than I would like, then I want them to grow up not only knowing their father well but also knowing that they are well loved. I want to get in better shape for them, because I would like them to see what a truly vital father looks like. And I have decided to read to them whenever they ask, if I possibly can. I do not have any memory of my father telling me, “No more books” at bedtime. I will forever picture him with an arm around me, holding a book out before me, showing me the world.

Thomas is the author of the debut novel,’We Are Not Ourselves’, out now.

 

Back tomorrow Jeanne

 

 

 

 

 

 

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About jeanne hambleton

Journalist-wordsmith, former reporter, columnist, film critic, editor, Town Clerk and then fibromite and eventer with 5 conferences done and dusted. Interested in all health and well being issues, passionate about research to find a cure and cause for fibromyalgia. Member LinkedIn. Worked for 4 years with FMA UK as Regional Coordinator for SW and SE,and Chair for FMS SAS the Sussex and Surrey FM umbrella charity and Chair Folly Pogs Fibromyalgia Research UK - finding funding for our "cause for a cure" and President and co ordinator of National FM Conferences. Just finished last national annual Fibromyalgia Conference Weekend. This was another success with speakers from the States . Next year's conference in Chichester Park Hotel, West Sussex, will be April 24/27 2015 and bookings are coming in from those who raved about the event every year. I am very busy but happy to produce articles for publication. News Editor of FMS Global News on line but a bit behind due to conference. A workaholic beyond redemption! The future - who knows? Open to offers with payment. Versatile and looking for a regular paid column - you call the tune and I will play the pipes.
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