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|By Amy Yee Pouring a bucket of ice water over one’s head may seem like a distant summer memory. But although the “ice bucket challenge” craze has died down, public awareness of amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrig’s disease, has never been stronger. The viral video campaign raised $115 million from more than 3 million donors for the ALS Association. In one month, from July 29 to August 29, donors raised $100.9 million, compared with $2.8 million during the same period the previous year. In early October, the ALS Association began spending that money. It approved $21.7 million of funding for six programs and initiatives by groups that include the academic-industry partnership ALS Accelerated Therapeutics, the New York Genome Center, three California labs that form the Neuro Collaborative, and Project MinE, which will map the genomes of 15,000 people with ALS (about 10 percent of ALS patients have a family member with the disease). The grants focus on developing gene therapies for common ALS genes and exploring approaches to counter two major contributors to the disease, the inflammation of nervous tissue and misfolded proteins in brain cells that control movement. These efforts may not only someday lead to new treatments, but may also point to the cause of ALS. At the level of basic research, scientists do not have a dominant theory from which to work, notes Tom Jessell, a neuroscientist and co-director of Columbia University’s new Zuckerman Mind Brain Behavior Institute. Jessell is also the chair of the research advisory board of Project ALS, a nonprofit that identifies and funds ALS research. © 2014 Scientific American
By Roni Caryn Rabin When I was in college, my father David started walking with an odd, barely perceptible limp. He was in his mid-40s, a gregarious physician, teacher and researcher who was always upbeat. He told his four kids that he had a “back problem” — a deliberately vague cover story that I, for one, was willing to believe. I had never heard of the real culprit — amyotrophic lateral sclerosis, or A.L.S. In fact, no one had. A.L.S. was a disease in the shadows. During my father’s life, it didn’t even have its own advocacy organization. This was the early ’80s, long before support groups and the Internet and a colored ribbon for every cause. And it was way before ice bucket challenges. My parents continued to use their code — “back problem” — to talk about the disease. They used it to protect my younger sisters, who were about to start high school, but I think they were also protecting themselves. My mother was also a physician, and they both knew exactly what lay ahead. Saying “A.L.S.” out loud was too threatening. But soon there was no getting around it. My father’s legs were getting weaker, his muscles were wasting, and he started relying on a cane to get around. I was 19, and my mother and I were out running errands one afternoon when she pulled the car over to the curb and stopped. She told me the truth. This was no slipped disc. She laid it all out for me in black and white: A.L.S. is a progressive, degenerative neurological disease that causes paralysis in the entire body. It’s fatal. There is no cure. It sounded like something from a horror movie. Over the next five years, as my father’s health deteriorated, he remained remarkably determined. He ate a high-protein diet and swam laps every day in an attempt to maintain his muscle and fend off the atrophy caused by the disease. He kept on swimming laps in our next-door neighbor’s pool, even when he had to use a walker — and later a wheelchair — to get there. © 2014 The New York Times Company
By GRETCHEN REYNOLDS Amyotrophic lateral sclerosis has been all over the news lately because of the ubiquitous A.L.S. ice bucket challenge. That attention has also reinvigorated a long-simmering scientific debate about whether participating in contact sports or even vigorous exercise might somehow contribute to the development of the fatal neurodegenerative disease, an issue that two important new studies attempt to answer. Ever since the great Yankees first baseman Lou Gehrig died of A.L.S. in 1941 at age 37, many Americans have vaguely connected A.L.S. with athletes and sports. In Europe, the possible linkage has been more overtly discussed. In the past decade, several widely publicized studies indicated that professional Italian soccer players were disproportionately prone to A.L.S., with about a sixfold higher incidence than would have been expected numerically. Players were often diagnosed while in their 30s; the normal onset is after 60. These findings prompted some small, follow-up epidemiological studies of A.L.S. patients in Europe. To the surprise and likely consternation of the researchers, they found weak but measurable associations between playing contact sports and a heightened risk for A.L.S. The data even showed links between being physically active — meaning exercising regularly — and contracting the disease, raising concerns among scientists that exercise might somehow be inducing A.L.S. in susceptible people, perhaps by affecting brain neurons or increasing bodily stress. But these studies were extremely small and had methodological problems. So to better determine what role sports and exercise might play in the risk for A.L.S., researchers from across Europe recently combined their efforts into two major new studies. The results should reassure those of us who exercise. The numbers showed that physical activity — whether at work, in sports or during exercise — did not increase people’s risk of developing A.L.S. © 2014 The New York Times Company
By ZACH SCHONBRUN EAST RUTHERFORD, N.J. — Victor Cruz dumped a bucket of ice water on his head at home on Sunday and then stepped out on thin ice himself — challenging the Giants’ co-owners to do the same. Taking part in the Ice Bucket Challenge — a social media craze that raises awareness for Lou Gehrig’s disease (amyotrophic lateral sclerosis) — Cruz, a wide receiver, posted the video on his Twitter feed. “That water was cold, man,” Cruz said Monday. The Ice Bucket Challenge was started by friends and family members of Pete Frates, a 29-year-old from Beverly, Mass., who played baseball at Boston College and was found to have A.L.S., a neurodegenerative condition, in 2012. As a reward for withstanding the icy punishment, the participant gets to nominate another person, who has 24 hours to complete the task. Cruz aimed high, calling out the co-owners John Mara and Steve Tisch to step under the bucket themselves. Just before practice on Monday, the 59-year-old Mara, wearing a white Giants T-shirt and black shorts, allowed Cruz to dump a Gatorade tub filled with ice water over his head. Before doing so, Mara nominated the Jets’ owner, Woody Johnson; the Patriots’ owner, Robert K. Kraft; and Patriots Coach Bill Belichick to do the same. “Feels good,” a smiling Mara said in a video posted on the Giants’ team website. It is unclear if Tisch will follow suit. Those who fail to complete the task within 24 hours are asked to donate to A.L.S. research. © 2014 The New York Times Company
By Bill Briggs A Vietnam veteran swoops his hand through a row of baby vegetables, caressing the peppers on down to the kale. The plants are aligned in tidy, military order atop his backyard fence. He could spend hours describing his first garden. But he cannot utter a word. He can’t even eat his eventual harvest. So, Bob Hoaglan, 71, simply stands and grins at the spouts behind his Oxnard, Calif., home. Then, he grabs his primary communication tool, an LCD tablet, scribbling a stylus across the screen. He displays his words with a silent chuckle: “I don’t have a green thumb.” With a button click, he erases that sentence before composing another. His daily aim is to throw his body and brain into new pursuits. The crops — fresh life for a man facing mortality — help shove his disease to the back of his mind. He admits, though, he can’t keep it there: “I try,” he writes, “Sometimes it creeps up on me.” As he shows that message, the smile vanishes. Hoaglan was diagnosed with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, nearly a year ago. Inside a malady that offers no cure or explanation, he embodies two intriguing clues that, a top researcher says, may whisper answers: Hoaglan served in the military, and he is a nice man. U.S. veterans carry a nearly 60 percent greater risk of contracting ALS than civilians, according to a white paper published in 2013 by the ALS Association, citing Harvard University research that tracked ex-service members back to 1910.
New findings reveal how a mutation, a change in the genetic code that causes neurodegeneration, alters the shape of DNA, making cells more vulnerable to stress and more likely to die. The particular mutation, in the C9orf72 gene, is the most common cause for amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease), and frontotemporal degeneration (FTD), the second most common type of dementia in people under 65. This research by Jiou Wang, Ph.D., and his colleagues at Johns Hopkins University (JHU) was published in Nature and was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS). In ALS, the muscle-activating neurons in the spinal cord die, eventually causing paralysis. In FTD neurons in particular brain areas die leading to progressive loss of cognitive abilities. The mutation may also be associated with Alzheimer’s and Huntington’s diseases. DNA contains a person’s genetic code, which is made up of a unique string of bases, chemicals represented by letters. Portions of this code are divided into genes that provide instructions for making molecules (proteins) that control how cells function. The normal C9orf72 gene contains a section of repeating letters; in most people, this sequence is repeated two to 25 times. In contrast, the mutation associated with ALS and FTD can result in up to tens of thousands of repeats of this section.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 19328 - Posted: 03.06.2014
By LAUREN BRADY When I was 18 I watched my father perform what would be his final surgery. It was the summer of 2007 and I had just returned to Colorado after surviving my freshman year of film school at New York University. One day my dad invited me to observe a vitrectomy. And while I hadn’t a clue what this would entail I immediately accepted, honored by the invitation and determined not to faint. My father’s 21 years as an ophthalmologist produced over 15,000 operations, a private practice spanning three offices, and very little vacation time. While I sensed from an early age that the long hours were taxing on him I never felt an absence. In fact, my childhood was picturesque: two loving parents, a rowdy little brother whom I pushed around until he was big enough to push back, family trips in the Jeep to the Rocky Mountains. He was the dad with the Handycam at every soccer game and school play. He worked as a surgeon, but he lived for his children. The morning of the vitrectomy we left extra early because of a limp in my dad’s right leg that had appeared a few months earlier and had gradually worsened. He suspected it was a pinched nerve and had been meaning to get it checked out. In the interim, he had started using a chair during surgery. Walking toward the hospital entrance we encountered a fellow doctor who greeted me with the familiarity of someone who’d been exposed to years of my father’s wallet photos. He asked how I liked Greenwich Village, whether I had directed any films yet and if I had tried a bialy. We walked and talked until I noticed at one point that my dad was no longer part of the conversation. Turning around I realized he was a half block back pushing himself up from the ground. © 2014 The New York Times Company
By KATIE HAFNER While undressing for bed one night in 2009, Susan Spencer-Wendel noticed that the muscles in her left palm had disappeared, leaving a scrawny pile of tendons and bones. Her right hand was fine. She let out a yelp and showed the hand to her husband, who told her to go to the doctor. She was 42. Ms. Spencer-Wendel then entered a protracted period of denial. Adopted as an infant in Florida, she traveled from her home in West Palm Beach to find blood relatives living in Cyprus, who confirmed that there was no family history of her worst fear: amyotrophic lateral sclerosis, or A.L.S., the relentless disease that lays waste to muscles while leaving the mind intact. In June 2011, a doctor in Miami gave her a definitive diagnosis of A.L.S., smiling “like he was inviting me to a birthday party,” she writes in “Until I Say Goodbye: My Year of Living With Joy.” Patients with A.L.S., which is also known as Lou Gehrig’s disease, typically live no more than four years after the onset of symptoms. There is no cure. Ms. Spencer-Wendel thought she had prepared herself fully — that she would burst off the starting block like a sprinter to greet her fate. Instead, when she heard the news, “I dropped my head for the start ... and began to cry.” Her heart-ripping book chronicles what she did immediately after her diagnosis: she decided to embrace life while death chased her down. Instead of letting the world close in on her, she resolved to travel as far and as wide for as long as she could. She went to the Yukon with her best friend, Budapest with her husband, and the Bahamas with her sister. © 2013 The New York Times Company
by Emily Underwood Globs of protein clustered in the neurons that control muscles have long been the hallmark of amyotrophic lateral sclerosis (ALS), the fatal neurodegenerative disease also commonly known as Lou Gehrig's disease. Now, a study of the most commonly found mutant gene in people with ALS reveals an unexpected origin of some of those sticky masses, a finding that may offer drug developers a new target for treatments. Located on the ninth chromosome, which explains part of its unwieldy name, the C9orf72 gene has a bit of a stutter. A typical version in healthy people contains a stretch of DNA where a string of six genetic letters—GGGGCC—repeats up to 25 times. Scientists have recently found that in a sizable share of people with ALS and frontotemporal dementia (FTD), a less common neurological disease characterized by language, memory, and emotional problems, this repeat occurs many more times; some people have thousands of copies. Since these C9orf72 mutations were discovered in 2011, some researchers have speculated that the repeats interrupt production of the gene's normal protein, which serves some as-yet unknown, but vital function in motor neurons or other brain cells. Others have hypothesized that the mutation spawns a large, misshapen strand of RNA that grabs on to proteins such as TDP-43, which normally help process RNA, creating protein tangles that starve the cell of the machinery it needs to function. © 2010 American Association for the Advancement of Science
By KATIE HAFNER SEATTLE — Dr. Richard Wesley has amyotrophic lateral sclerosis, the incurable disease that lays waste to muscles while leaving the mind intact. He lives with the knowledge that an untimely death is chasing him down, but takes solace in knowing that he can decide exactly when, where and how he will die. Under Washington State’s Death With Dignity Act, his physician has given him a prescription for a lethal dose of barbiturates. He would prefer to die naturally, but if dying becomes protracted and difficult, he plans to take the drugs and die peacefully within minutes. “It’s like the definition of pornography,” Dr. Wesley, 67, said at his home here in Seattle, with Mount Rainier in the distance. “I’ll know it’s time to go when I see it.” Washington followed Oregon in allowing terminally ill patients to get a prescription for drugs that will hasten death. Critics of such laws feared that poor people would be pressured to kill themselves because they or their families could not afford end-of-life care. But the demographics of patients who have gotten the prescriptions are surprisingly different than expected, according to data collected by Oregon and Washington through 2011. Dr. Wesley is emblematic of those who have taken advantage of the law. They are overwhelmingly white, well educated and financially comfortable. And they are making the choice not because they are in pain but because they want to have the same control over their deaths that they have had over their lives. © 2012 The New York Times Company
Researchers have linked newly discovered gene mutations to some cases of the progressive fatal neurological disease amyotrophic lateral sclerosis — ALS, also known as Lou Gehrig’s disease. Shedding light on how ALS destroys the cells and leads to paralysis, the researchers found that mutations in this gene affect the structure and growth of nerve cells. ALS attacks motor neurons, the nerve cells responsible for controlling muscles. People with ALS experience such early symptoms as limb weakness or swallowing difficulties. In most people, the disease leads to death three to five years after symptoms develop, usually as a result of respiratory failure. Scientists at the University of Massachusetts Medical School, Worcester, collaborated with international ALS researchers to search for gene mutations in two large families with an inherited form of ALS. The researchers used a technique to decode only the protein-encoding portions of DNA, known as the exome, allowing an efficient yet thorough search of the DNA regions most likely to contain disease-causing mutations. This deep sequencing of the exome led to the identification of several different mutations in the gene for profilin (PFN1) which were present only in the family members that developed ALS. Further investigations of 272 other familial ALS cases across the world showed that profilin mutations were also found in a small subset (about 1 to 2 percent) of the familial ALS cases studied. The protein profilin is a key part of the creation and remodeling of a nerve cell's scaffolding or cytoskeleton. In fly models, disrupting profilin stunts the growth of axons — the long cell projections used to relay signals from one neuron to the next or from motor neurons to muscle cells. After identifying the PFN1 mutations in ALS patients, the researchers demonstrated that these mutations inhibited axon growth in laboratory-grown motor neurons as well. They also found that mutant profilin accumulated in clumps in neural cells, as has been seen for other abnormal proteins associated with ALS, Parkinson's and Alzheimer's.
By Erica Westly Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, is a progressive neuromuscular disease that affects about 130,000 people worldwide a year. The vast majority of patients are isolated cases with no known family history of the disease. They usually start developing symptoms of the loss of motor neurons in middle age and die within five years of diagnosis. Researchers know very little about what causes ALS. Now a recent study in Nature Biotechnology suggests that the neuron death associated with the disease may be caused by astrocytes, a type of brain cell that normally helps neurons. Previous research had suggested that astrocytes could become toxic in the rare form of ALS known to have genetic roots, and the study authors wanted to see if a similar phenomenon might happen in the more common isolated cases. The answer turned out to be yes: when they cultured astrocytes from those ALS patients, the healthy motor neurons in the culture began to die off after a few days. Other types of neurons were unaffected by the astrocytes, suggesting that they specifically harm the neurons involved in controlling the body’s movements. Lead author Brian Kaspar, a neuroscientist at Ohio State University, and his collaborators next will attempt to figure out what makes the astrocytes behave this way. If researchers can understand why motor neurons die in ALS, they may have a better chance of finding a cure. © 2012 Scientific American,
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 16298 - Posted: 01.26.2012
By Katherine Harmon Stephen Hawking turns 70 on Sunday, beating the odds of a daunting diagnosis by nearly half a century. The famous theoretical physicist has helped to bring his ideas about black holes and quantum gravity to a broad public audience. For much of his time in the public eye, though, he has been confined to a wheelchair by a form of the motor-neuron disease amyotrophic lateral sclerosis (ALS). And since 1985 he has had to speak through his trademark computer system—which he operates with his cheek—and have around-the-clock care. But his disease seems hardly to have slowed him down. Hawking spent 30 years as a full professor of mathematics at the University of Cambridge. And he is currently the director of research at the school's Center for Theoretical Cosmology. But like his mind, Hawking's illness seems to be singular. Most patients with ALS—also known as Lou Gehrig's disease, for the famous baseball player who succumbed to the disease—are diagnosed after the age of 50 and die within five years of their diagnosis. Hawking's condition was first diagnosed when he was 21, and he was not expected to see his 25th birthday. Why has Hawking lived so long with this malady when so many other people die so soon after diagnosis? We spoke with Leo McCluskey, an associate professor of neurology and medical director of the ALS Center at the University of Pennsylvania, to find out more about the disease and why it has spared Hawking and his amazing brain. © 2012 Scientific American,
By AMANDA SCHAFFER Ever since the New York Yankees Hall of Famer Lou Gehrig benched himself in 1939, never to return to the game, the ailment that now bears his name has stoked dread in the American imagination. Lou Gehrig’s disease — also known as amyotrophic lateral sclerosis, or A.L.S. — has afflicted well-known figures like the jazz great Charles Mingus, the physicist Stephen Hawking and the historian Tony Judt. The disease stems from the progressive deterioration of nerve cells, leading to a loss of control over voluntary muscles, difficulty breathing and swallowing, creeping paralysis and eventually death. There is no cure and no good treatment. Scientists are still unsure exactly what causes most cases. But in the journal Nature last week, researchers at Northwestern University identified a possible culprit: a cellular housekeeping agent that normally helps cells to clear away proteins that are damaged or misfolded. When the housekeeper fails, proteins seem to aggregate inside nerve cells, which may be contributing to their destruction. The finding has been hailed as a breakthrough by patient groups and scientists. The new work is “fueling great enthusiasm and interest,” said Dr. Amelie Gubitz of the National Institute of Neurological Disorders and Stroke, which helped finance the new work. Still, it is far from clear that this is the wellspring of A.L.S. There are at least a dozen processes that also might contribute to the demise of motor nerve cells, Dr. Gubitz noted. © 2011 The New York Times Company
A breakdown of a recycling system in cells appears to be the underlying cause of a fatal nerve disease. Amyotrophic lateral sclerosis (ALS), the most common form of motor neuron disease, causes paralysis. A US team, writing in Nature, found the flaw in the way nerve cells in the brain recycle protein building blocks, which means cells cannot repair themselves and become damaged. Experts in the UK said that the findings were significant. ALS affects an estimated 350,000 people around the world, including children and adults, with about half of people dying within three years of its onset. The breakdown occurs in the recycling system in the nerve cells of the spinal cord and the brain. In order to function properly, the protein building blocks in the cells need to be recycled. But in ALS, that system is broken. The cell cannot repair or maintain itself and becomes severely damaged. The scientists found a protein, ubiquilin2, which should be directing the recycling process, does not work in people with ALS. BBC © 2011
People who smoke cigarettes or have smoked in the past may be more likely to develop Lou Gehrig's disease, according to a new study. The disease slowly kills the neurons that send messages between the brain and the rest of the body, causing patients to lose control of their muscles -- including those that are essential for eating and breathing. Most people who are diagnosed with Lou Gehrig's disease, also known as amyotrophic lateral sclerosis, or ALS, don't survive more than five years after the diagnosis. About 20,000 to 30,000 people in the United States have ALS, according to the Centers for Disease Control and Prevention. While about 10 percent of those cases are caused by a genetic defect, the rest have no known cause. Some previous studies have suggested that smoking may be one factor that increases a person's risk of getting ALS, but others have found no link. "Results have been rather conflicting regarding the association between smoking and ALS," said Dr. Fang Fang, who has investigated the question at the Karolinska Institute in Stockholm, Sweden, but was not involved with the current study. Many ALS researchers tend to agree on a positive association between cigarette smoking and ALS risk although some quite-recent studies still report no link, he told Reuters Health in an e-mail. In the current study, researchers led by Dr. Hao Wang of the Harvard School of Public Health collected data from five long-term studies in the United States that altogether included more than a million adults. In all of the studies, participants had been asked if they currently smoked or had smoked in the past, and if so, how frequently and for how many years. Copyright 2011 Thomson Reuters.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 15008 - Posted: 02.15.2011
By BINA VENKATARAMAN BOSTON — Tracking the inexorable advance of amyotrophic lateral sclerosis, the deadly neuromuscular ailment better known as Lou Gehrig’s disease or A.L.S., has long been an inexact science — a matter of monitoring weakness and fatigue, making crude measurements of the strength of various muscles. This imprecision has hindered the search for drugs that could slow or block the disease’s progress. But now a neurologist at Beth Israel Deaconess Medical Center here has won a $1 million prize — reportedly the largest ever for meeting a specific challenge in medical research — for developing a reliable way to quantify the small muscular changes that signal progressive deterioration. The winner, Dr. Seward Rutkove, showed that his method could cut in half the cost of clinical trials to screen potential drugs for the disease, said Melanie Leitner, chief scientific officer of Prize4Life, the nonprofit group that created the competition. The method does not provide a target in the body at which to aim drugs, nor will it help doctors better diagnose the disease. But Dr. Merit Cudkowicz, a professor of neurology at Massachusetts General Hospital and a chairwoman of the Northeast A.L.S. Consortium, compared Dr. Rutkove’s discovery to the way magnetic resonance imaging expedited the development of drugs for multiple sclerosis. “You can use this as a tool to screen drugs to see if they will affect survival,” she said, but added, “The ultimate prize is finding a drug that works for A.L.S.” © 2011 The New York Times Company
by Deborah Kotz No question that a diagnosis of Lou Gehrig's disease -- as former Massachusetts governor Paul Cellucci announced Thursday -- is devastating. The disease, amyotrophic lateral sclerosis, or ALS, targets the brain and spine, causing muscle weakness that progresses to complete paralysis. There's no cure, and it's always fatal, usually within a decade of diagnosis. Yet Cellucci, who's currently the US ambassador to Canada, says his ALS is progressing slowly: "I've had symptoms for four years," the 62-year-old told the Associated Press. He said he has some muscle weakness, but other than that, he's "feeling quite well." Of course, one of the most famous ALS sufferers, besides Lou Gehrig himself, is physicist and cosmologist Stephen Hawking, who was diagnosed with the disease more than 45 years ago and is still living despite decades of complete paralysis. Some experts, though, say Hawking doesn't have true ALS but a similar type of motor neuron disease that progresses much more slowly. Unfortunately, no test can provide a definitive diagnosis of ALS, according to the National Institute of Neurological Disorders and Stroke. Doctors make the diagnosis based on symptoms by looking at loss of nerve function in the limbs and ruling out other more common diseases.They also look for progression of symptoms over time. © 2011 NY Times Co.
By ALLEN G. BREED JACKSONVILLE, N.C. — As she walked through the door, Sabrina Parker's big hazel eyes flared with surprise and she raised a hand to her mouth to stifle a gasp. She was a huge fan of the "Twilight" book and movie series, and her friends and family had transformed this greasy garage into a Sweet 16's dream. Homemade strobe lights illuminated walls decorated like the night sky and plastered with cast posters. All around were balloons in red, white and black. An enormous cake, iced to look like the chess board on one of the book jackets, held 16 blazing candles. The crowd began chanting for Sabrina to blow them out. She bent in close and blew, but the flames barely flickered. She straightened up and shook her head. Realizing her distress, Matt Scozzari stepped closer and told her they would do it together. On the count of three, they leaned in and snuffed them out together. In the three months since he'd first asked her out, Matt had noticed small changes in his girlfriend: The shortness of breath, the slurring in her speech, the weight loss. When he'd ask what was going on, Sabrina would just shrug it off as nothing serious. But Sabrina knew her condition was very serious. About a month after she started seeing Matt, Sabrina learned that she had amyotrophic lateral sclerosis, also known as Lou Gehrig's Disease — the same illness that had killed her mother and grandmother. A doctor told Sabrina it wouldn't be long before she would have to decide whether to go on a ventilator. Copyright 2010 The Associated Press.
By Kay Lazar New research suggests that athletes who have had multiple head injuries, and possibly others such as military veterans exposed to repetitive brain traumas, may be prone to developing a disabling neurological disease similar to amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig’s disease. A team of researchers from Boston University School of Medicine and the Veterans Administration Hospital in Bedford said yesterday they have pinpointed evidence of a new disease that mimics ALS in the brains of two former National Football League players previously thought to have died of ALS. They also found the new disease in the brain of a deceased professional boxer who was a military veteran. In most cases, ALS strikes people — many in the prime of life — with no apparent rhyme or reason. The progressive nerve disorder, which affects an estimated 30,000 Americans, slowly paralyzes patients while leaving their mind intact. But if this early research is borne out by autopsies of additional athletes and veterans, it would support the idea that an ALS-type illness can be triggered by the traumas of sports and war. “We believe that these three cases are the tip of the iceberg,’’ said neurosurgeon Robert Cantu, who is a codirector of the BU Center for the Study of Traumatic Encephalopathy. “We don’t know whether this is linked to the increased incidence of ALS in the military, who are subject to blasts and other head injuries, but we are concerned that it may be.’’ The findings, the authors speculated, could mean that athletes and some others previously diagnosed with ALS actually had the related syndrome — perhaps even Gehrig himself, the New York Yankees star who is the iconic ALS sufferer. It’s a mystery that will never be solved, however, because Gehrig’s body was cremated. © 2010 NY Times Co
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 15: Language and Our Divided Brain
Link ID: 14379 - Posted: 08.20.2010