About Us
Founded in 1944, the American Committee for the Weizmann Institute of Science develops philanthropic support for the Weizmann Institute in Israel, and advances its mission of science for the benefit of humanity.
Jan 17, 2007... REHOVOT, ISRAEL—January 17, 2007—An injury to the brain can be devastating. When brain cells die, whether from head trauma, stroke or disease, a substance called glutamate floods the surrounding areas, overloading the cells in its path and setting off a chain reaction that damages whole swathes of tissue. Glutamate is always present in the brain, where it carries nerve impulses across the gaps between cells. But when this chemical is released by damaged or dying brain cells, the result is a flood that overexcites nearby cells and kills them.
Jul 16, 2019...
Photo of neurosurgery from healthline.com
If you’re ever unfortunate enough to require brain surgery, Israeli startup Nurami Medical has got you covered – literally.
The Haifa-based company has developed a patch made of synthetic, biodegradable nanofibers meant to be affixed to the dura mater – the protective membrane underneath the skull that keeps the brain and spinal cord safe – after cranial neurosurgery.
Oct 27, 2017...
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The placebo effect is best known in medicine for making people feel better when they are given sham treatments. Now there is growing interest in using placebos to boost athletic and cognitive abilities.
Previous studies have found that people lift more weight and cycle harder when they take medicines with no active ingredients that are falsely labelled as performance-enhancing substances. Placebo pills have also been shown to improve scores in memory tests.
Jan 09, 2019...
Illustration by Jess Rodrigues via Shutterstock.com
Israeli researchers recently made a discovery that could help develop new therapies for anxiety disorders. With up to one in three people around the world at the risk of experiencing severe anxiety, this is big news.
At the heart of the discovery, published in Cell Reports, is a previously unknown biochemical pathway underlying anxiety.
Researchers from the Weizmann Institute of Science biomolecular sciences department studied the role of proteins called importins in the central nervous system (the brain and spinal cord). Importins are found in all cells. Their job is to shuttle molecules into the nucleus.
Oct 29, 2014... In his role as part of the science and modern dance performance at Lincoln Center, Prof. Elad Schneidman describes how he is ""learning to read the language of the brain"" – revealing how the brain makes words, sentences, paragraphs. As he speaks, dancers move about him – as individuals, then building on their connections – in an interpretation of this language.
May 21, 2017...
A researcher works with stem cells in a laboratory. (photo credit :REUTERS)
Dr. Valery Krizhanovsky is a modern Juan Ponce de Leon, looking for a Fountain of Youth. The Weizmann Institute molecular biologist is not, however, seeking an anti-aging cure for wrinkles but a way to eliminate senescent cells in various organs of the body to delay or prevent age-related diseases. Born in the southeastern part of the Ukraine as an only child, Krizhanovsky studied at pharmacy school in the Russian city of Kursk. Fortunately for science, he never completed his studies there due to technical reasons. His father, an aeronautics engineer, and his mother, a dentist, accompanied him at the age of 20 to Israel to settle. Not interested in becoming a physician, he completed his first degree in nutrition at the Hebrew University’s Faculty of Agriculture, Food and Environment and then conducted research and earned his master’s degree. He then returned to HU for his doctoral study with developmental biology Prof. Nissim Ben-Arie on the genetics of the nervous system. Krizanovsky did post-doctoral studies at the Cold Spring Harbor Lab in New York, an internationally renowned research institute whose researchers included Dr. James D. Watson, co-discoverer of DNA’s double helix, and seven other Nobel Prize laureates. Then he returned to Weizmann as a researcher and lecturer. His wife works in on the administrative side of science in the field of grants for research. Their two daughters, age 13 and 10, are too young to consider a career. “We want them to do things that interest them and that they are the best in,” he said in very fluent, accented Hebrew that he learned almost completely in Israel. “I have focused on the molecular cell biology of aging; it interested me from early on. I am very satisfied here. There are excellent students and a good atmosphere. I have eight or nine people working in my lab,” he said in an interview with The Jerusalem Post. He will present his work at the MIXiii Biomed conference, May 23-25, in Tel Aviv, which is dedicated this year to aging and age related diseases. Few laymen – or even scientists – know much about the multidisciplinary subject of cellular senescence; to some the term may bring to mind the obsolescence of smartphones. Senescence comes from the Latin for “to grow old” and is a natural cellular response that can be trigged by damage to the DNA and other factors. Eventually, it will probably be dealt with in the future by stimulating the immune system to attack the unwanted cells. In fact, cellular senescence is a programmed state in which the stable cell cycle is halted. Cellular senescence is now considered a fundamental cell process playing important physiological roles in embryonic development, wound healing and tumor suppression, but ironically, it is also involved in pathophysiological conditions including age-related diseases, notably cancer and degenerative diseases such as sarcopenia, atherosclerosis, Parkinson’s disease and Alzheimer’s disease. As such, research on therapeutic strategies in the field, said Krizhanovsky, has gained tremendous momentum. Last year, he organized a meeting of the Cell Senescence Association at Weizmann in Rehovot, and some 200 scientists attended. This year’s conference has just been held in Paris. SOME LAYMEN have heard the simplistic idea that aging is the result of the shortening of telomeres, a kind of cap at the end of each chromosome that protects it deterioration or from fusion with neighboring chromosomes. They are like the plastic tips at the end of shoelaces that, when the coating deteriorates and frays, they no longer function. Without telomeres, the DNA strands become damaged and the cells can’t function properly. “Telomeres getting shorter can be one of reasons for aging, but it is not the central one. The main cause of aging is a combination of a lot of factors that can happen simultaneously and at different levels – molecular, physical and physiological,” explained Krizhanovsky. “The telomeres in mice are very long and don’t get shorter, but that doesn’t make them live any longer. Senescent cells, which stop dividing, accumulate in the tissue. I do all my research on mice or on human tissue in the lab. Just as senescent cells accumulate in the tissue of mice, they accumulate in the tissues of people. We assess them quantitatively.” Mice can live for about two and a half years, some maybe more. There is another rodent model that can live for 35 years underground. They live in the north and are called naked mole rats. “They don’t get cancer but rather die of old age. We don’t work on them, but I believe there is a lab at Haifa’s Technion-Israel Institute of Technology that study them.” He doesn’t know about senescent cells in insects or birds, but they do exist in other mammals and in fish. Senescent cells accumulate in mammalian organisms as they get older, he explained, and they are present in sites of age-related diseases. While senescence aids embryonic development and limits the transformation of cells into cancer cells, the presence of senescent cells in tissues of the adult organism can also promote the appearance of tumors, a decline in tissue function and tissue aging. “When senescent cells gradually accumulate in tissues they promote a chronic ‘sterile’ inflammation, a hallmark of unhealthy aging. Several genetic studies in mice suggest that the elimination of senescent cells from the organism leads to extension of the mouse’s health span and lifespan. So, drugs allowing the efficient elimination of senescent cells in the mouse is a promising strategy for treatment of age-related diseases associated with accumulation of senescent cells. “We eliminate senescent cells from mice using this pharmacological approach and study the effects of such elimination on the aging of the organism as a whole and on specific age-related diseases. A few age-related diseases account for most of the causes of death in old people. Senescent cells accumulate in premalignant lesions, sites of tissue damage and in normal tissues during aging. We study the effect of the elimination of senescent cells in mouse models of these diseases. One of these diseases, chronic obstructive pulmonary disease, mostly involves chronic lung inflammation and is one of the leading causes of death in humans,” he said. HIS TEAM studies the positive link between epithelial cell senescence and progression of chronic lung diseases. “Altogether, these studies focus on elimination of senescent cells as a promising strategy for extension of health span and lifespan as well as directed treatment of age-related diseases and to uncover the molecular mechanisms of the effect of senescent cells on these conditions.” When the senescent cells stop dividing, they become pro-inflammatory, release cytokines, enzymes and other things that change the cells’ environment and are not good for the tissue. The immune system has to be called in to kill them off. The tissue cannot return to the state that existed before the damage was done.” Until around 2005, when several articles published in Nature showed that senescent cells can prevent the development of malignant tumors, this field of research was very limited, recalled the Weizmann researcher. “We don’t understand the process. Maybe when we do, we’ll be able to prevent the development of a premalignant growth into a cancerous tumor.” THE FIRST description of senescent cells, said Krizhanovsky, was made by Prof. Leonard Hayflick, an expert in anatomy at the school of medicine of University of California at San Francisco who was a professor of medical microbiology at the Stanford University School of Medicine. Hayflick, who marked his 89th birthday yesterday (May 20), has studied the aging process for more than three decades. In 1961, he discovered that human cells divide for a limited number of times in a controlled environment outside a living being; his discovery became known as the “Hayflick limit.” For a few decades, not many people were interested in the field of cellular senescence, and it was hard to get funding for research. Those Israelis who do post-doctoral research usually do it in the US, and there was skepticism about senescent cells, so only a few labs there studied the subject. But there were a number of very good labs in Europe – in Germany, the Netherlands, Spain, England, and now at the Pasteur Institute in France that actively pursued it.” Their work piqued the interest of researchers in the US as well, and the field got a boost. Although the Krizhanovsky lab does not conduct experiments on patients, “we cooperate with doctors, too, including some at Meir Medical Center in Kfar Saba and Hadassah University Medical Center in Jerusalem.” Senescent cells “look different” than other cells that keep dividing. They are large and flat, as if they were eroded, like a yolk in an egg. As they accept blue tinted liquid, it looks like a blue fried egg, he said. “They can be found in every type of tissue that divides naturally, such as the skin, digestive system, the lungs, kidneys, skin and hair. But we know very little about their existence in the heart or the brain,” he went on. “We want to understand why they don’t die on their own. There is an apparatus involving the amount of protein in them that prevents death of the cells [apoptosis]. When we reduce the amount of proteins, the cells die. We could administer chemicals to kill them, but there are side effects that can cause more damage than benefit.” Senescent cells accumulate in the skin. “If we kill them, there is a rise in the division of progenitor cells, thus this could cause more renewal of skin cells, he suggested. As for baldness, senescent cell research could contribute significantly, as it may be that if they are eliminated, hair grows. It has been done in mice in a lab in the Netherlands.” He doesn’t know if the elimination of senescent cells in humans will make them look young. “There are a lot of promises at this stage, but my lab is focusing on diseases connected to aging. This will make it possible to extend longevity and the number of years people are healthy. People live longer today than they did a century ago because nutrition is better, there are statins to reduce cholesterol in the blood, we have antibiotics to deal with bacteria and fewer people smoke. People’s telomeres are not longer today than they were in 1900, but humankind lives longer because there are better conditions.” The Weizmann scientist predicts than in another five to 10 years, “the understanding of senescent cells will produce clinical treatment in patients – probably not in cancer patients, but in those suffering from diseases connecting to aging like osteoarthritis. Such medications – pills or injections – would have to be given once in a while, not daily. “In the meantime, we have to understand more from basic research.”
https://www.weizmann-usa.org/news-media/feature-stories/understanding-alzheimer-s/
Jun 28, 2010... One in 10 Americans over the age of 65 has Alzheimer's disease, a debilitating neurological disorder that slowly destroys memory and cognitive function and for which there is no cure. According to the National Institutes of Health (NIH), because the risk of developing the disease increases with age and more people are living longer, the number of people suffering from Alzheimer's is likely to grow dramatically over the next few decades. Despite years of research by scientists all over the world, Alzheimer's is still poorly understood.
Apr 24, 2018...
Neuroscientist Michael Heneka knows that radical ideas require convincing data. In 2010, very few colleagues shared his belief that the brain’s immune system has a crucial role in dementia. So in May of that year, when a batch of new results provided the strongest evidence he had yet seen for his theory, he wanted to be excited, but instead felt nervous.
He and his team had eliminated a key inflammation gene from a strain of mouse that usually develops symptoms of Alzheimer’s disease. The modified mice seemed perfectly healthy. They sailed through memory tests and showed barely a sign of the sticky protein plaques that are a hallmark of the disease. Yet Heneka knew that his colleagues would consider the results too good to be true.
https://www.weizmann-usa.org/news-media/in-the-news/blood-test-for-alzheimer-s/
Feb 04, 2013...
A simple blood test could be on the way for diagnosing Alzheimer’s disease. Image via Shutterstock.com*
“Today one of the main weaknesses in the Alzheimer’s area is that patients don’t find out until it’s too late,” says Ilya Budik, CEO of NeuroQuest, an Israeli company developing a novel blood test for early detection of the most common cause of dementia worldwide.
“There are many new therapies under development, and the most successful trials are showing the earlier a patient is treated, the better likelihood of responding to the treatment,” he says.
Mar 20, 2019... REHOVOT, ISRAEL—March 20, 2019—A shot of espresso, a piece of chocolate, or a headstand – all of these have been recommended before taking a big test. The best advice, however, could be to take a deep breath. According to research conducted in the lab of Prof. Noam Sobel of the Weizmann Institute of Science’s Department of Neurobiology, people who inhaled when presented with a visuospatial task were better at completing it than those who exhaled in the same situation. The results of the study, which were published in Nature Human Behavior, suggest that the olfactory system may have shaped the evolution of brain function far beyond the basic function of smelling.
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