Amyotrophic Lateral Sclerosis Press Releases: National Institute of Neurological Disorders and Stroke (NINDS)

Stem cells have been hailed as a toolkit to treat a host of diseases, but at an NIH symposium on May 6, researchers said they are still deciphering the toolkit’s instruction manual.

Star-shaped support cells in the brain secrete a toxin that kills motor neurons in a model of amyotrophic lateral sclerosis (ALS), two new studies show. The studies may lead to new ways of diagnosing and treating the disorder.

Researchers at the National Institutes of Health (NIH) have completed the first large-scale study of the role of common genetic variation in sporadic amyotrophic lateral sclerosis (ALS), which occurs in people without any family history of the disease. The results provide interesting hints about the causes of the disorder and can serve as a starting point for future studies.

Using microarray technology, researchers supported by the National Institutes of Health (NIH) have shown that people with one variant of a gene that’s active in the brain have better episodic memory – the ability to remember events and facts – than do people without that variant. The researchers are using the same technology to identify genetic risk factors associated with neurological diseases.

Increasing the amount of a specific enzyme in the brain partially restores memory in a mouse model for Alzheimer’s disease (AD), researchers say. The results could eventually lead to new treatments for AD or other neurodegenerative disorders.

The National Institute of Neurological Disorders and Stroke (NINDS) has appointed six new members to its major advisory panel, the National Advisory Neurological Disorders and Stroke Council. The NINDS, a component of the National Institutes of Health (NIH), is the nation’s primary supporter of basic, translational, and clinical research on the brain and nervous system. NINDS Director Story Landis, Ph.D., formally introduced the new members, who will serve through July 2010, at the Council’s September 14, 2006 meeting.

Six outstanding scientists who target neurological disorders at the cellular and molecular level were recently awarded the prestigious Senator Jacob Javits Award in the Neurosciences. The award provides for up to seven years of research funding from the National Institute of Neurological Disorders and Stroke (NINDS), the nation’s leading agency for research on the brain and nervous system and a component of the National Institutes of Health.

For the first time, researchers have enticed transplants of embryonic stem cell-derived motor neurons in the spinal cord to connect with muscles and partially restore function in paralyzed animals. The study suggests that similar techniques may be useful for treating such disorders as spinal cord injury, transverse myelitis, amyotrophic lateral sclerosis (ALS), and spinal muscular atrophy. The study was funded in part by the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).

A new study in mice suggests that Alzheimer's disease (AD) may be triggered when adult neurons try to divide. The finding helps researchers understand what goes wrong in the disease and may lead to new ways of treating it.

Most people with a rare type of dementia called primary progressive aphasia (PPA) have a specific combination of prion gene variants, a new study shows. The study is the first to link the prion protein gene to this disorder. The researchers also looked at the prion protein gene in people with Alzheimer's disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease) and did not find any association with specific gene variants in those disorders.

While several treatments are currently available for Alzheimer's disease (AD), none of them can slow or halt the course of this devastating disorder. In a new study, researchers have now identified three compounds that inhibit an enzyme believed to be involved in the process that leads to AD. This discovery may lead to new treatments that can stop the disease process in its tracks.

The National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health, has named six scientists to receive its prestigious Senator Jacob Javits Award in the Neurosciences. The award is given to individual investigators who have demonstrated exceptional scientific excellence and productivity in research supported by the NINDS and who are expected to conduct innovative research over the next 7 years.

Four prominent investigators were recently awarded the prestigious Senator Jacob Javits Award in the Neurosciences, which provides for up to seven years of research funding from the National Institute of Neurological Disorders and Stroke (NINDS).

New research suggests that an off-the-market pain reliever called indoprofen may be a starting point for finding a new drug to treat spinal muscular atrophy (SMA), a devastating childhood neurological disorder.

A new study shows that a common antibiotic used to treat bacterial infections increases survival rates and delays nerve damage in a mouse model for amyotrophic lateral sclerosis (ALS). The antibiotic works by activating or "turning on" the gene encoding the glutamate transporter in neurons. This finding may lead to new drug treatments for ALS and other neurodegenerative diseases.

Eight noted investigators have been awarded the prestigious Senator Jacob Javits Award in the Neurosciences, which provides for up to seven years of research funding from the National Institute of Neurological Disorders and Stroke (NINDS). The award, which honors the late U.S. Senator Jacob Javits, is presented to investigators who have demonstrated exceptional scientific excellence and productivity in research areas supported by the NINDS and who are expected to conduct cutting-edge research over the next seven years.

Using a specially designed robotic microscope to study cultured cells, researchers have found evidence that abnormal protein clumps called inclusion bodies in neurons from people with Huntington's disease (HD) prevent cell death. The finding helps to resolve a longstanding debate about the role of these inclusion bodies in HD and other disorders and may help investigators find effective treatments for these diseases.
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Many neurological diseases occur when specific groups of neurons die because of nerve damage, toxins, inflammation, or other factors. A new study suggests that activity of a single gene can stop neurons from dying regardless of what triggers this process. The findings could lead to new ways of treating neurodegenerative diseases.
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Production of a growth factor in the spinal cord drops just before the onset of symptoms in an animal model of a rare, hereditary motor neuron disease, scientists have found. The findings point to a potential new way of treating this disease, and possibly other neurodegenerative disorders as well.
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The antibiotic minocycline delays onset and slows progression of symptoms in a mouse model for amyotrophic lateral sclerosis (ALS), a new study shows. The study also revealed that the drug may work by blocking release of a molecule that triggers cell death. The findings may lead to new ways of treating ALS or other neurodegenerative disorders.
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A new study shows that combining the supplement creatine and the antibiotic minocycline significantly slows disease progression and prolongs survival in a mouse model of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease.
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Researchers funded in part by the National Institute of Neurological Disorders and Stroke (NINDS) have identified the gene that causes a rare juvenile-onset form of amyotrophic lateral sclerosis (ALS). The discovery of the Senataxin gene, on chromosome 9q34, may provide clues to the mechanisms of related brain disorders.
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Officials at the National Institute of Neurological Disorders and Stroke (NINDS) hailed the identification of a gene associated with the familial form of ALS (Lou Gehrig's disease). "This discovery is extremely important because it marks the first identification of a specific gene for a neurodegenerative disease of adult life," said Carl M. Leventhal, M.D., director of the NINDS program that contributed to support for the research reported in the March 3 issue of Nature*. "It also suggests a likely mechanism for the damage to nerve cells in familial ALS and, possibly, other brain disorders."

A new study reveals for the first time how gene mutations lead to the inherited form of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. The study suggests that the two most prominent theories of how familial ALS (FALS) and other related diseases develop are both right in part.
Fact Sheet

Officials at the National Institute of Neurological Disorders and Stroke (NINDS) hailed as a major research advance the mapping of a gene that causes familial amyotrophic lateral sclerosis (ALS) to chromosome 21. "This is an important first step in our attempt to better understand the basic, molecular mechanisms of this widely studied but poorly understood neurological disorder," said Dr. Roger J. Porter, deputy director of the NINDS.
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For the first time, researchers have shown that an experimental vaccine can reduce the amount of neurodegeneration in a mouse model for Parkinson's disease. The finding suggests that a similar therapy might eventually be able to slow the devastating course of Parkinson's disease in humans.
Fact Sheet

Production of a growth factor in the spinal cord drops just before the onset of symptoms in an animal model of a rare, hereditary motor neuron disease, scientists have found. The findings point to a potential new way of treating this disease, and possibly other neurodegenerative disorders as well.
Fact Sheet

Researchers funded in part by the National Institute of Neurological Disorders and Stroke (NINDS) have identified the gene that causes a rare juvenile-onset form of amyotrophic lateral sclerosis (ALS). The discovery of the Senataxin gene, on chromosome 9q34, may provide clues to the mechanisms of related brain disorders.
Fact Sheet

A new study reveals for the first time how gene mutations lead to the inherited form of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. The study suggests that the two most prominent theories of how familial ALS (FALS) and other related diseases develop are both right in part.
Fact Sheet

A new study shows for the first time in humans that nerve cell transport problems could play a key role in the degeneration of motor neurons, the nerve cells that control movement. The finding is an important step toward understanding the biology of motor neuron diseases and could lead to the development of effective treatments.
Fact Sheet

A new study shows that combining the supplement creatine and the antibiotic minocycline significantly slows disease progression and prolongs survival in a mouse model of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease.
Fact Sheet

Many neurological diseases occur when specific groups of neurons die because of nerve damage, toxins, inflammation, or other factors. A new study suggests that activity of a single gene can stop neurons from dying regardless of what triggers this process. The findings could lead to new ways of treating neurodegenerative diseases.
Fact Sheet

The antibiotic minocycline delays onset and slows progression of symptoms in a mouse model for amyotrophic lateral sclerosis (ALS), a new study shows. The study also revealed that the drug may work by blocking release of a molecule that triggers cell death. The findings may lead to new ways of treating ALS or other neurodegenerative disorders.
Fact Sheet

Officials at the National Institute of Neurological Disorders and Stroke (NINDS) hailed the identification of a gene associated with the familial form of ALS (Lou Gehrig's disease). "This discovery is extremely important because it marks the first identification of a specific gene for a neurodegenerative disease of adult life," said Carl M. Leventhal, M.D., director of the NINDS program that contributed to support for the research reported in the March 3 issue of Nature*. "It also suggests a likely mechanism for the damage to nerve cells in familial ALS and, possibly, other brain disorders."

Officials at the National Institute of Neurological Disorders and Stroke (NINDS) hailed as a major research advance the mapping of a gene that causes familial amyotrophic lateral sclerosis (ALS) to chromosome 21. "This is an important first step in our attempt to better understand the basic, molecular mechanisms of this widely studied but poorly understood neurological disorder," said Dr. Roger J. Porter, deputy director of the NINDS.
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Many post-polio patients have swallowing abnormalities that increase the risk of choking but are unaware of their condition, according to a study directed by a scientist at the National Institute of Neurological Disorders and Stroke (NINDS) and published in the April 25 issue of the New England Journal of Medicine.*
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