Posts Tagged ‘medicine’


Prof Sarah Tabrizi , from the UCL Institute of Neurology, led the trials

By James Gallagher

The defect that causes the neurodegenerative disease Huntington’s has been corrected in patients for the first time, the BBC has learned. An experimental drug, injected into spinal fluid, safely lowered levels of toxic proteins in the brain. The research team, at University College London, say there is now hope the deadly disease can be stopped.

Experts say it could be the biggest breakthrough in neurodegenerative diseases for 50 years.

Huntington’s is one of the most devastating diseases. Some patients described it as Parkinson’s, Alzheimer’s and motor neurone disease rolled into one.

Peter Allen, 51, is in the early stages of Huntington’s and took part in the trial: “You end up in almost a vegetative state, it’s a horrible end.”

Huntington’s blights families. Peter has seen his mum Stephanie, uncle Keith and grandmother Olive die from it. Tests show his sister Sandy and brother Frank will develop the disease. The three siblings have eight children – all young adults, each of whom has a 50-50 chance of developing the disease.

The unstoppable death of brain cells in Huntington’s leaves patients in permanent decline, affecting their movement, behaviour, memory and ability to think clearly.

Peter, from Essex, told me: “It’s so difficult to have that degenerative thing in you.

“You know the last day was better than the next one’s going to be.”
Huntington’s generally affects people in their prime – in their 30s and 40s
Patients die around 10 to 20 years after symptoms start
About 8,500 people in the UK have Huntington’s and a further 25,000 will develop it when they are older

Huntington’s is caused by an error in a section of DNA called the huntingtin gene. Normally this contains the instructions for making a protein, called huntingtin, which is vital for brain development. But a genetic error corrupts the protein and turns it into a killer of brain cells.

The treatment is designed to silence the gene.

On the trial, 46 patients had the drug injected into the fluid that bathes the brain and spinal cord. The procedure was carried out at the Leonard Wolfson Experimental Neurology Centre at the National Hospital for Neurology and Neurosurgery in London. Doctors did not know what would happen. One fear was the injections could have caused fatal meningitis. But the first in-human trial showed the drug was safe, well tolerated by patients and crucially reduced the levels of huntingtin in the brain.

Prof Sarah Tabrizi, the lead researcher and director of the Huntington’s Disease Centre at UCL, told the BBC: “I’ve been seeing patients in clinic for nearly 20 years, I’ve seen many of my patients over that time die. For the first time we have the potential, we have the hope, of a therapy that one day may slow or prevent Huntington’s disease . This is of groundbreaking importance for patients and families.”

Doctors are not calling this a cure. They still need vital long-term data to show whether lowering levels of huntingtin will change the course of the disease. The animal research suggests it would. Some motor function even recovered in those experiments.

Peter, Sandy and Frank – as well as their partners Annie, Dermot and Hayley – have always promised their children they will not need to worry about Huntington’s as there will be a treatment in time for them. Peter told the BBC: “I’m the luckiest person in the world to be sitting here on the verge of having that. “Hopefully that will be made available to everybody, to my brothers and sisters and fundamentally my children.”

He, along with the other trial participants, can continue taking the drug as part of the next wave of trials. They will set out to show whether the disease can be slowed, and ultimately prevented, by treating Huntington’s disease carriers before they develop any symptoms.

Prof John Hardy, who was awarded the Breakthrough Prize for his work on Alzheimer’s, told the BBC: “I really think this is, potentially, the biggest breakthrough in neurodegenerative disease in the past 50 years. That sounds like hyperbole – in a year I might be embarrassed by saying that – but that’s how I feel at the moment.”

The UCL scientist, who was not involved in the research, says the same approach might be possible in other neurodegenerative diseases that feature the build-up of toxic proteins in the brain. The protein synuclein is implicated in Parkinson’s while amyloid and tau seem to have a role in dementias.

Off the back of this research, trials are planned using gene-silencing to lower the levels of tau.

Prof Giovanna Mallucci, who discovered the first chemical to prevent the death of brain tissue in any neurodegenerative disease, said the trial was a “tremendous step forward” for patients and there was now “real room for optimism”.

But Prof Mallucci, who is the associate director of UK Dementia Research Institute at the University of Cambridge, cautioned it was still a big leap to expect gene-silencing to work in other neurodegenerative diseases.

She told the BBC: “The case for these is not as clear-cut as for Huntington’s disease, they are more complex and less well understood. But the principle that a gene, any gene affecting disease progression and susceptibility, can be safely modified in this way in humans is very exciting and builds momentum and confidence in pursuing these avenues for potential treatments.”

The full details of the trial will be presented to scientists and published next year.

The therapy was developed by Ionis Pharmaceuticals, which said the drug had “substantially exceeded” expectations, and the licence has now been sold to Roche.

http://www.bbc.com/news/health-42308341

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Last year, doctors of optometry detected more than 320,000 cases of diabetes. Imagine if they could make the same impact when it comes to exposing early signs of Alzheimer’s disease.

November is National Alzheimer’s Disease Awareness Month. An estimated 5.4 million Americans are affected by Alzheimer’s disease, according to the Centers for Disease Control and Prevention (CDC). Projections put the number at 13.8 million by 2050.

Maryke Nijhuis Neiberg, O.D., associate professor in the School of Optometry at Massachusetts College of Pharmacy and Heath Sciences, in Worcester, Massachusetts, considers this an unrealized patient education opportunity for doctors of optometry.

“The earlier diagnoses give doctors and patients a better chance at managing the progressive brain disease and preserving the patient’s quality of life,” Dr. Neiberg says. “There has been some increase in Alzheimer’s awareness over the years, particularly in the eye community, but not enough yet.

“Alzheimer’s is a significant future public health issue,” she adds. “It is still a terminal disease.”

Early intervention

Much of the research on Alzheimer’s disease seeks to slow the disease’s progression. For instance, a study in Biological Psychiatry on Nov. 6 by researchers at the University of Iowa and the University of Texas Southwestern Medical Center in Dallas reports that there may be a new treatment that can slow the depression and cognitive decline associated with Alzheimer’s disease, without affecting amyloid plaque deposits or reactive glia in rats.

Among the early signs of Alzheimer’s, the researchers say, are anxiety, depression and irritability-long before the devastating effects of memory loss.

“Thus, P7C3 compounds may form the basis for a new class of neuroprotective drugs for mitigating the symptoms in patients with Alzheimer’s disease by preserving neuronal cell survival, irrespective of other pathological events,” researchers say. “P7C3 compounds represent a novel route to treating depression, and new-onset depression in elderly patients may herald the development of Alzheimer’s disease with later cognitive impairments to follow.”

Another study in JAMA Ophthalmology in September by researchers at Stanford University and Veterans Affairs Palo Alto Health Care System linked visual impairment and cognition in older adults and also stressed the “potential importance” of vision screening in identifying these patients’ eye disease and cognitive deficits. The AOA strongly recommends comprehensive eye examinations and stresses the limitations of screenings.

Optometry’s role

According to the CDC:

The rate of Alzheimer’s jumped 50 percent between 1999 and 2014.

Americans fear losing their mental capacity more than losing their physical abilities.

More than $230 billion is estimated to be spent in 2017 on providing health care, long-term care, hospice plus unpaid care for relatives with Alzheimer’s and other dementias.

More large-scale research on Alzheimer’s needs to be done, but progress is being made. Dr. Neiberg pointed to research linking optical coherence tomography (OCT) of the macula to Alzheimer’s and Parkinson’s diseases.

“With the advent of OCT, we now know that the retinal ganglion cell layer thins and that the optic nerve cup-to-disc ratio increases in size, not unlike glaucoma,” Dr. Neiberg says. “Alzheimer’s produces visual field defects that are easily confused with glaucoma. What we need is large-scale research to determine how much of the normal tension glaucoma we diagnose and treat is ultimately related to Alzheimer’s disease.”

She adds, “The early perceptual changes that occur in early Alzheimer’s are startling and measurable. One of the earliest signs is a decline in the Benton Visual Retention Test, a test of visual memory. This test requires the duplication of shapes on paper with a pencil, and is scored.

“Research has shown that this test is able to predict high risk for Alzheimer’s 15 years before diagnosis,” she says. “It’s a simple test many developmental and pediatric optometrists already have on their shelves. If we combine that test and the ocular findings we see, we have a very strong indication that something is indeed amiss. Armed with this information, the patient can then consult with their primary care physician, initiate lifestyle modification and request a referral if necessary.”

There is no cure for Alzheimer’s disease. But doctors of optometry can engage patients in conversation about Alzheimer’s disease and how they can manage their own risk factors, including:

Smoking
Mid-life obesity
Sedentary lifestyle
High-cholesterol diet|
Vascular disease (i.e., diabetes and hypertension)

“Lifestyle modification and early access to medication, which can delay the progression of dementia, might be enough to keep the disease at bay for longer,” Dr. Neiberg says. “We should include the Alzheimer’s disease connection when we educate our patients about lifestyle diseases.”

https://finchannel.com/society/health-beauty/69483-doctors-of-optometry-can-spot-early-signs-of-alzheimer-s-disease


A one-time intravenous infusion of the high dose of gene therapy at Nationwide Children’s Hospital in Ohio extended the survival of patients with spinal muscular atrophy type 1 (SMA1) in a Phase 1 clinical trial, according to a study.

A one-time intravenous infusion of the high dose of gene therapy extended the survival of patients with spinal muscular atrophy type 1 (SMA1) in a Phase 1 clinical trial, according to a study published in the New England Journal of Medicine. The study was conducted by Researchers from Nationwide Children’s Hospital in collaboration with AveXis, Inc. and The Ohio State University College of Medicine.

“My team at Nationwide Children’s has worked with commitment and dedication to develop a therapy that may subsequently be shown through future clinical trials to potentially alter the course of this unforgiving condition and provide a therapeutic option for the families and infants with SMA1,” says Jerry Mendell, MD, principal investigator in the Center for Gene Therapy at Nationwide Children’s.

SMA1 is a progressive, childhood, neuromuscular disease caused by a mutation in a single gene. Children with SMA1 fail to meet motor milestones and typically die or require permanent mechanical ventilation by 2 years of age. The phase 1 clinical trial is the first to test the functional replacement of the mutated gene responsible for SMA1.

A one-time intravenous injection of modified adeno-associated virus serotype 9 (AAV9) delivered the SMN gene to 15 patients. Three patients received a low dose, while 12 patients received a high dose. In the Phase 1 trial, patients in the high dose group demonstrated improvement in motor function and they had a decreased need for supportive care compared to the natural history of the disease.

Specifically, at the end of the study period, all 15 patients appeared to have a favorable safety profile and to be generally well tolerated. Of the 12 patients treated with the high dose, 92 percent of patients have achieved head control, 75 percent of patients can roll over and 92 percent of patients can sit with assistance. Seventy-five percent of these patients are now sitting for 30 seconds or longer. Two patients can crawl, pull to stand and stand and walk independently.

According to natural history of the disease, patients require nutritional and respiratory support by 12 months of age, and are not able to swallow or speak effectively. Of the patients who received the high dose in study, 11 patients are able to speak, 11 patients are fed orally and seven do not require bi-level positive airway pressure as of the data cut-off (August 7, 2017).

“In this first phase of clinical trials, we have observed preliminary results that appear to be promising compared to the natural history of SMA Type 1,” says Dr. Mendell, also a faculty member at The Ohio State University College of Medicine.

This study builds on nearly three decades of foundational research led by teams at Nationwide Children’s and Ohio State’s Wexner Medical Center and exemplifies the strong basic science and clinical bonds between the two institutions. Arthur Burghes, PhD, of Ohio State created a ground-breaking SMA mouse model that remains the standard by which all therapies, including AVXS-101, are initially tested. Senior author of the study, Brian Kaspar, PhD, during his appointment at Nationwide Children’s discovered that the AAV9 vector was capable of crossing the blood brain barrier when injected into the vascular system to deliver genes directly to motor neurons. The two laboratories then collaborated to show that scAAV9-SMN, when delivered to SMA mice shortly after birth, completely prevented their neuromuscular disorder. The laboratories also collaborated to successfully prove that reversing a protein deficiency through gene therapy is effective in improving and stabilizing SMA in a large animal model. “In neurological disease, it is rare to go from gene defect to therapy so directly, and the fact that this has happened here in one place is perhaps even rarer,” said John Kissel, MD, chair of Neurology at Ohio State and director of the SMA Clinic at Nationwide Children’s.

AveXis, Inc., a clinical-stage gene therapy company developing treatments for patients suffering from rare and life-threatening neurological genetic diseases, announced in July 2016 that the U.S. Food and Drug Administration (FDA) granted Breakthrough Therapy Designation for the treatment based on preliminary clinical results from the trial of AVXS-101.

“At AveXis, we are enormously pleased to see that all children who received AVXS-101 are alive and free of permanent ventilatory support at 20 months of age and older — an age where, sadly, only eight percent of untreated children with SMA Type 1 are expected to survive without permanent breathing support,” said Dr. Kaspar, now serving as Chief Scientific Officer at AveXis. “The New England Journal of Medicine publication marks an exciting milestone in the development of AVXS-101.”

Journal Reference:

Jerry R. Mendell, Samiah Al-Zaidy, Richard Shell, W. Dave Arnold, Louise R. Rodino-Klapac, Thomas W. Prior, Linda Lowes, Lindsay Alfano, Katherine Berry, Kathleen Church, John T. Kissel, Sukumar Nagendran, James L’Italien, Douglas M. Sproule, Courtney Wells, Jessica A. Cardenas, Marjet D. Heitzer, Allan Kaspar, Sarah Corcoran, Lyndsey Braun, Shibi Likhite, Carlos Miranda, Kathrin Meyer, K.D. Foust, Arthur H.M. Burghes, Brian K. Kaspar. Single-Dose Gene-Replacement Therapy for Spinal Muscular Atrophy. New England Journal of Medicine, 2017; 377 (18): 1713 DOI: 10.1056/NEJMoa1706198

By SAM ROBERTS

Julius Youngner, an inventive virologist whose nearly fatal childhood illness destined him to become a medical researcher and a core member of the team that developed the Salk polio vaccine in 1955, died on April 27 at his home in Pittsburgh. He was 96.

His death was confirmed by his son, Dr. Stuart Youngner.

Dr. Youngner was the last surviving member of the original three-man research team assembled by Dr. Jonas Salk at the University of Pittsburgh to address the polio scourge, which peaked in the United States in the early 1950s when more than 50,000 children were struck by it in one year. Three other assistants later joined the group.

Dr. Salk credited his six aides with major roles in developing the polio vaccine, a landmark advance in modern medicine, which he announced on April 12, 1955.

The announcement — that the vaccine had proved up to 90 percent effective in tests on 440,000 youngsters in 44 states — was greeted with ringing churchbells and openings of public swimming pools, which had been drained for fear of contagion. Within six years, annual cases of the paralyzing disease had declined from 14,000 to fewer than 1,000.

By 1979, polio had been virtually eliminated in developed nations.

“I think it’s absolutely fair to say that had it not been for Dr. Youngner, the polio vaccine would not have come into existence,” Dr. Salk’s son, Peter L. Salk, president of the Jonas Salk Legacy Foundation and a visiting professor at the University of Pittsburgh Graduate School of Public Health, said in an email.

While Dr. Youngner, who was 34 at the time, remained at the university and made further advances in virology, he and other members of the team remained embittered that Dr. Salk had not singled them out for credit in his announcement speech.

The printed version was prefaced with the phrase “From the Staff of the Virus Research Laboratory by Jonas E. Salk, M.D.,” and a United Press account quoted him as crediting his original three assistants, who had joined him as early as 1949 — Dr. Youngner, Army Maj. Byron L. Bennett and Dr. L. James Lewis — as well as three others.

“The really important thing to recognize is that the development of the polio vaccine at the University of Pittsburgh was a team effort,” Dr. Peter Salk wrote.

He added, “There is no question that my father recognized the importance of the team, and if there were circumstances in which that wasn’t adequately expressed, I would feel that it needs to be expressed now and very clearly so.”

In 1993, Dr. Youngner crossed paths with Dr. Salk for the first time since Dr. Salk left for California in 1961. According to “Polio: An American Story” (2005), by David M. Oshinsky, Dr. Youngner raised the 1955 announcement speech in confronting Dr. Salk.

“Do you remember whom you mentioned and whom you left out?” the book quoted him as saying to Dr. Salk. “Do you realize how devastated we were at that moment and ever afterward when you persisted in making your co-workers invisible?”

Asked later, though, whether he regretted having worked for Dr. Salk, Dr. Youngner replied: “Absolutely not. You can’t imagine what a thrill that gave me. My only regret is that he disappointed me.”

Dr. Youngner’s contribution to the team was threefold.

He developed a method called trypsinization, using monkey kidney cells to generate sufficient quantities of the virus for experiments and production of the vaccine. He also found a way to deactivate the virus without disrupting its ability to produce antibodies. And he created a color test to measure polio antibodies in the blood to determine whether the vaccine was working.

He later contributed research to understanding interferon as an antiviral agent in the treatment of cancer and hepatitis; to the development (with Dr. Samuel Salvin) of gamma interferon, which is used against certain infections; and to advances that resulted in vaccines for Type A influenza and (with Dr. Patricia Dowling) equine influenza.

“As a direct result of his efforts, there are countless numbers of people living longer and healthier lives,” Dr. Arthur S. Levine, the University of Pittsburgh’s senior vice chancellor for the health sciences and dean of its medical school, said in a statement.

Julius Stuart Youngner was born on Oct. 24, 1920, in Manhattan and raised in the Bronx, where he survived lobar pneumonia, a severe infection of the lungs. His father, Sidney Donheiser, was a businessman. His mother was Bertha Youngner. He took her surname when his parents divorced.

After graduating from Evander Childs High School in the Bronx at 15, he earned a bachelor’s degree in English with a minor in biology from New York University in 1939 and a master’s and doctorate of science in microbiology from the University of Michigan.

Drafted into the Army in World War II, he worked on the Manhattan Project at Oak Ridge, Tenn., and at the University of Rochester, testing the toxicity of uranium salts. He said he learned of the project’s goal of building an atomic bomb only when it was dropped on Japan.

He was working at the National Cancer Institute, part of the National Institutes of Health, when the University of Pittsburgh hired him as an assistant professor in 1949 to assist Dr. Salk. He was a professor of microbiology and medical genetics at the university School of Medicine and chairman of the department of microbiology (biochemistry and microbiology were added later) from 1966 until his retirement in 1989.

His first wife, the former Tula Liakakis, died in 1963. Besides their son, Stuart, a psychiatry and bioethics professor at Case Western Reserve University in Cleveland, Dr. Youngner is survived by his wife, the former Rina Balter; a daughter, Lisa, an artist, also from his first marriage; three grandchildren; and a half brother, Alan Donheiser.

Dr. Youngner’s infectious curiosity, as a colleague characterized it, generated hundreds of scholarly papers and more than 15 patents. He was president of the American Society for Virology from 1986 to 1987.

When he was 7, Dr. Youngner nearly died from the pneumonia he had contracted when bacteria ate through his chest and infected a rib. An effective vaccine for pneumonia and antibiotics would not be invented for nearly two decades.

“So they strapped my legs to a table, and two nuns held my arms and another held my head and they prayed while they operated on me,” he recalled in an oral history interview in the early 1990s with the National Council of Jewish Women. “To this day I can remember the feeling of the saw on that rib.

“Later in life, when I had to have some minor surgery,” he said, “I put it off for years because I was so affected by this episode.”

https://mobile.nytimes.com/2017/05/04/science/julius-youngner-dead-salk-polio-vaccine-researcher.html?_r=0&referer=https://www.google.com/

To create a new drug, researchers have to test tens of thousands of compounds to determine how they interact. And that’s the easy part; after a substance is found to be effective against a disease, it has to perform well in three different phases of clinical trials and be approved by regulatory bodies.

It’s estimated that, on average, one new drug coming to market can take 1,000 people, 12-15 years, and up to $1.6 billion. Here is a short video on the current process.

Last week, researchers published a paper detailing an artificial intelligence system made to help discover new drugs, and significantly shorten the amount of time and money it takes to do so.

The system is called AtomNet, and it comes from San Francisco-based startup AtomWise. The technology aims to streamline the initial phase of drug discovery, which involves analyzing how different molecules interact with one another—specifically, scientists need to determine which molecules will bind together and how strongly. They use trial and error and process of elimination to analyze tens of thousands of compounds, both natural and synthetic.

AtomNet takes the legwork out of this process, using deep learning to predict how molecules will behave and how likely they are to bind together. The software teaches itself about molecular interaction by identifying patterns, similar to how AI learns to recognize images.

Remember the 3D models of atoms you made in high school, where you used pipe cleaners and foam balls to represent the connections between protons, neutrons and electrons? AtomNet uses similar digital 3D models of molecules, incorporating data about their structure to predict their bioactivity.

As AtomWise COO Alexander Levy put it, “You can take an interaction between a drug and huge biological system and you can decompose that to smaller and smaller interactive groups. If you study enough historical examples of molecules…you can then make predictions that are extremely accurate yet also extremely fast.”

“Fast” may even be an understatement; AtomNet can reportedly screen one million compounds in a day, a volume that would take months via traditional methods.

AtomNet can’t actually invent a new drug, or even say for sure whether a combination of two molecules will yield an effective drug. What it can do is predict how likely a compound is to work against a certain illness. Researchers then use those predictions to narrow thousands of options down to dozens (or less), focusing their testing where there’s more likely to be positive results.

The software has already proven itself by helping create new drugs for two diseases, Ebola and multiple sclerosis. The MS drug has been licensed to a British pharmaceutical company, and the Ebola drug is being submitted to a peer-reviewed journal for additional analysis.

https://singularityhub.com/2017/05/07/drug-discovery-ai-can-do-in-a-day-what-currently-takes-months/

Thanks to Kebmodee for bringing this to the It’s Interesting community.

By Vanessa Bates Ramirez

In recent years, technology has been producing more and more novel ways to diagnose and treat illness.

Urine tests will soon be able to detect cancer: https://singularityhub.com/2016/10/14/detecting-cancer-early-with-nanosensors-and-a-urine-test/

Smartphone apps can diagnose STDs:https://singularityhub.com/2016/12/25/your-smartphones-next-big-trick-to-make-you-healthier-than-ever/

Chatbots can provide quality mental healthcare: https://singularityhub.com/2016/10/10/bridging-the-mental-healthcare-gap-with-artificial-intelligence/

Joining this list is a minimally-invasive technique that’s been getting increasing buzz across various sectors of healthcare: disease detection by voice analysis.

It’s basically what it sounds like: you talk, and a computer analyzes your voice and screens for illness. Most of the indicators that machine learning algorithms can pick up aren’t detectable to the human ear.

When we do hear irregularities in our own voices or those of others, the fact we’re noticing them at all means they’re extreme; elongating syllables, slurring, trembling, or using a tone that’s unusually flat or nasal could all be indicators of different health conditions. Even if we can hear them, though, unless someone says, “I’m having chest pain” or “I’m depressed,” we don’t know how to analyze or interpret these biomarkers.

Computers soon will, though.

Researchers from various medical centers, universities, and healthcare companies have collected voice recordings from hundreds of patients and fed them to machine learning software that compares the voices to those of healthy people, with the aim of establishing patterns clear enough to pinpoint vocal disease indicators.

In one particularly encouraging study, doctors from the Mayo Clinic worked with Israeli company Beyond Verbal to analyze voice recordings from 120 people who were scheduled for a coronary angiography. Participants used an app on their phones to record 30-second intervals of themselves reading a piece of text, describing a positive experience, then describing a negative experience. Doctors also took recordings from a control group of 25 patients who were either healthy or getting non-heart-related tests.

The doctors found 13 different voice characteristics associated with coronary artery disease. Most notably, the biggest differences between heart patients and non-heart patients’ voices occurred when they talked about a negative experience.

Heart disease isn’t the only illness that shows promise for voice diagnosis. Researchers are also making headway in the conditions below.

ADHD: German company Audioprofiling is using voice analysis to diagnose ADHD in children, achieving greater than 90 percent accuracy in identifying previously diagnosed kids based on their speech alone. The company’s founder gave speech rhythm as an example indicator for ADHD, saying children with the condition speak in syllables less equal in length.
PTSD: With the goal of decreasing the suicide rate among military service members, Boston-based Cogito partnered with the Department of Veterans Affairs to use a voice analysis app to monitor service members’ moods. Researchers at Massachusetts General Hospital are also using the app as part of a two-year study to track the health of 1,000 patients with bipolar disorder and depression.
Brain injury: In June 2016, the US Army partnered with MIT’s Lincoln Lab to develop an algorithm that uses voice to diagnose mild traumatic brain injury. Brain injury biomarkers may include elongated syllables and vowel sounds or difficulty pronouncing phrases that require complex facial muscle movements.
Parkinson’s: Parkinson’s disease has no biomarkers and can only be diagnosed via a costly in-clinic analysis with a neurologist. The Parkinson’s Voice Initiative is changing that by analyzing 30-second voice recordings with machine learning software, achieving 98.6 percent accuracy in detecting whether or not a participant suffers from the disease.
Challenges remain before vocal disease diagnosis becomes truly viable and widespread. For starters, there are privacy concerns over the personal health data identifiable in voice samples. It’s also not yet clear how well algorithms developed for English-speakers will perform with other languages.

Despite these hurdles, our voices appear to be on their way to becoming key players in our health.

https://singularityhub.com/2017/02/13/talking-to-a-computer-may-soon-be-enough-to-diagnose-illness/?utm_source=Singularity+Hub+Newsletter&utm_campaign=14105f9a16-Hub_Daily_Newsletter&utm_medium=email&utm_term=0_f0cf60cdae-14105f9a16-58158129

By Cari Romm

You may have heard of foreign-accent syndrome, a rare and mysterious condition in which someone suffers a brain injury and suddenly — true to the name — begins speaking in a new accent. Last year, for example, a woman from Ontario began speaking in the regional accent of the Canadian East Coast after a stroke, despite the fact that she’d never visited or met anyone from that particular part of the country. Just a few months ago, a woman in Texas developed a British accent following dental surgery.

Both women are members of a pretty exclusive club: Scientists estimate that foreign-accent syndrome strikes just one person in the world each year. And as Time reported earlier this week, a Georgia high-school student has taken the step further: Sixteen-year-old Rueben Nsemoh, recently woke up from a coma speaking fluent Spanish.

The patient: Last month, Nsemoh developed a severe concussion during a soccer game, when another player accidentally kicked him in the head. When he woke up after three days in a coma, according to Time, he’d lost his English, but he could still speak: His first words were “tengo hambre,” Spanish for “I’m hungry” — and his family quickly discovered that he could now speak the language fluently, despite the fact that he had previously known only a handful of Spanish words.

The diagnosis: This isn’t the first time a patient has walked away from a head injury with a newfound linguistic ability: In 2014, an Australian man came to and discovered that he now spoke fluent Mandarin; in 2010, the same thing happened to a Croatian teen with German and a British man with French.

But these cases, like Nsemoh’s, can’t simply be explained as an extension of foreign-accent syndrome, which researchers believe isn’t really the development of a new accent at all: It’s a sign of damage to the area of the brain that controls the motor functions of speech. Any resemblance to a real foreign accent, then, is coincidental — the new speech pattern is just a new way of forcing words out of the mouth, affecting their sounds in random ways.

Seemingly absorbing an entire language overnight, on the other hand, has little to do with motor skills and everything to do with linguistic knowledge. While Nsemoh’s family hasn’t yet received an explanation for his newfound grasp of Spanish, Time noted that he’s heard the language in the past, from his brother (who studied abroad in Spain) and his classmates, meaning it’s not entirely new. For now, that remains just a clue, though the teen’s doctors may not have much longer to solve the case — for the past few weeks, their patient has been slowly regaining his English and losing his Spanish. This one, it seems, may remain un misterio for the ages.