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Category: neuroscience

A state-of-the-art brain-machine interface created by UC San Francisco neuroscientists can generate natural-sounding synthetic speech by using brain activity to control a virtual vocal tract—an anatomically detailed computer simulation including the lips, jaw, tongue, and larynx. The study was conducted in research participants with intact speech, but the technology could one day restore the voices of people who have lost the ability to speak due to paralysis and other forms of neurological damage.

Stroke, , and such as Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease) often result in an irreversible loss of the ability to speak. Some people with severe speech disabilities learn to spell out their thoughts letter-by-letter using assistive devices that track very small eye or facial muscle movements. However, producing text or synthesized speech with such devices is laborious, error-prone, and painfully slow, typically permitting a maximum of 10 words per minute, compared to the 100–150 words per minute of natural speech.

The new system being developed in the laboratory of Edward Chang, MD—described April 24, 2019 in Nature—demonstrates that it is possible to create a synthesized version of a person’s voice that can be controlled by the activity of their ’s speech centers. In the future, this approach could not only restore fluent communication to individuals with severe speech disability, the authors say, but could also reproduce some of the musicality of the human voice that conveys the speaker’s emotions and personality.

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A special focus on rogue proteins may hold future promise in stopping the progression of nerve cell destruction in people who have amyotrophic lateral sclerosis (ALS) or frontotemporal dementia.

ALS, a rare but devastating disorder that’s also known as Lou Gehrig’s disease, attacks the body’s , resulting in progressive muscle weakness as the neurons degenerate over time. There is no cure. People with ALS eventually lose their strength and the ability to move their arms, legs and body.

About a third of those with ALS also develop frontotemporal dementia (FTD), a destruction of neurons in the brain that causes profound personality changes and disability. The two diseases are similar in both pathology and genetics. FTD tends to affect people earlier than Alzheimer’s disease, the most common type of dementia.

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Using human cancer cells, tumor and blood samples from cancer patients, researchers at Johns Hopkins Medicine have uncovered the role of a neurotransmitter in the spread of aggressive cancers. Neurotransmitters are chemical “messengers” that transmit impulses from neurons to other target cells.

The work, described in the April 9 issue of the journal Cell Reports, found that this neurotransmitter, called N-acetyl-aspartyl-glutamate (NAAG) NAAG is more abundant in cancers with a tendency to grow and spread rapidly—or so-called higher grade cancers—than in lower grade tumors, making it a potential marker for tumor progression or regression during cancer therapy, the researchers say. The experiments also demonstrated that NAAG is a source of glutamate, a chemical that cancer cells use as building blocks to survive, in tumors that express an enzyme called glutamate carboxypeptidase II (GCPII). The group also discovered that stopping the GCPII from being active by using a drug called 2-PMPA to treat human ovarian tumors implanted in ovaries of mice, reduced tumor weights and glutamate concentrations.

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O.o its prob gonna eat me someday :0.

Slime mould might easily be one of the strangest life forms on our planet. They are neither plants, animals, nor fungi, but various species of complex, single-celled amoebas of the protist kingdom. Sometimes they form colonies able to grow, move, and even exhibit a strange kind of intelligence.

Even without a nervous system, they are able to learn about substances they encounter, retaining that knowledge and even communicating it to other slime moulds. Now a team of scientists at the French National Centre for Scientific Research (CNRS) has figured out how: slime moulds actually absorb the substance into their veins.

Researchers at the CNRS’ Centre for Research on Animal Cognition conducted their experiments on a fascinating little fellow called Physarum polycephalum, a single-celled blob with multiple nuclei, and a popular candidate for studying slime mould intelligence. (Here you can see it navigate a maze. Cool!)

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The spoken word is a powerful tool, but not all of us have the ability to use it, either due to biology or circumstances. In such cases, technology can bridge the gap — and now that gap is looking shorter than ever, with a new algorithm that turns messages meant for your muscles into legible sounds.

Converting the complex mix of information sent from the brain to the orchestra of body parts required to transform a puff of air into meaningful sound is by no means a simple feat.

The lips, tongue, throat, jaw, larynx, and diaphragm all need to work together in near-perfect synchrony, requiring our brain to become a master conductor when it comes to uttering even the simplest of phrases.

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Researchers are edging closer to a therapy for Angelman syndrome that involves injecting molecules that can edit genes into the fetal brain. They have already succeeded in mice and say the approach could eventually treat people with the syndrome.

The work is of high interest because a similar strategy could also work for other genetic conditions linked to autism.

But the prospect of injecting molecules into fetal brains poses ethical questions, experts caution.

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Worldwide, 50 million people are living with Alzheimer’s disease and other dementias. According to the Alzheimer’s Association, every 65 seconds someone in the United States develops this disease, which causes problems with memory, thinking and behavior.

It has been more than 100 years since Alois Alzheimer, M.D., a German psychiatrist and neuropathologist, first reported the presence of senile plaques in an Alzheimer’s patient brain. It led to the discovery of that produces deposits or plaques of fragments in the brain, the suspected culprit of Alzheimer’s disease. Since then, amyloid has been extensively studied because of its association with Alzheimer’s disease. However, amyloid precursor protein distribution within and on neurons and its function in these cells remain unclear.

A team of neuroscientists led by Florida Atlantic University’s Brain Institute sought to answer a fundamental question in their quest to combat Alzheimer’s disease—” Is amyloid precursor protein the mastermind behind Alzheimer’s disease or is it just an accomplice?”

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In multiple sclerosis, the body’s immune system attacks and damages myelin, which is the insulating layer on nerves in the spinal cord, brain and optic nerve. This causes the nerves to short-circuit and cease functioning properly. In “a potential game-changer,” scientists have now demonstrated that a synthetic molecule can restore compromised myelin.

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