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Amyotrophic Lateral Sclerosis (ALS) Press Releases

Mutation blocks nuclear transport

Nuclear transport problems linked to ALS and FTD
Friday, Oct 16, 2015
Three teams of scientists supported by the National Institutes of Health showed that a genetic mutation linked to some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) may destroy neurons by disrupting the movement of materials in and out of the cell’s nucleus, or command center where most of its DNA is stored.

Viral genes in ALS

Dormant viral genes may awaken to cause ALS
Wednesday, Sep 30, 2015
Scientists at the National Institutes of Health (NIH) discovered that reactivation of ancient viral genes embedded in the human genome may cause the destruction of neurons in some forms of amyotrophic lateral sclerosis (ALS).

Cellular energy factories

PINK1 protein crucial for removing broken-down energy reactors
Wednesday, Aug 12, 2015
Cells are powered by tiny energy reactors called mitochondria. When damaged, they leak destructive molecules that can cause substantial harm and eventually kill brain cells. Scientists at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) showed that a protein called PINK1 that is implicated in Parkinson’s disease is critical for helping cells get rid of dysfunctional mitochondria.

New NIH logo

NIH announces grants for frontotemporal degeneration research
Thursday, Oct 23, 2014
The National Institutes of Health will award three large, five-year projects on a specific form of dementia, known as frontotemporal because of the areas of the brain that are affected. The projects, funded by the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), National Institute on Aging (NIA) and the National Center for Advancing Translational Sciences (NCATS), announced today total more than $5.9 million for 2014.

Lariats may reduce TDP-43 toxicity by clustering with TDP-43.

Genetic Lassos May Steer Neurons Toward Survival During Lou Gehrig's Disease
Wednesday, Apr 10, 2013
Cowboys use lassos to catch runaway horses and cattle. Recently, NINDS-funded researchers showed that genetic lassos may also be used to “round-up” toxic runaway molecules in neurons. Their results suggest that molecules, called RNA lariats, may effectively prevent nerve degeneration during amyotrophic lateral sclerosis.

Human iPS cells differentiating into dopaminergic neurons

Patient-derived stem cells could improve drug research for Parkinson's
Wednesday, Jul 4, 2012
Researchers have taken a step toward better drug therapies for Parkinson's disease and Huntington's disease by investigating signs of distress and vulnerability in patient-derived cells. Cells derived from patients with Parkinson's had different responses to drug treatments depending on the type of Parkinson's each patient had. These are the latest advances from the NINDS iPS cell consortia.

A DNA helix

Genetic mutation linked to inherited forms of ALS, dementia
Wednesday, Sep 28, 2011
Researchers have identified the most common genetic cause known to date for two neurological diseases, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). A mutation in a single gene on chromosome 9 accounts for nearly 50 percent of familial ALS and FTD in Finland, and more than a third of familial ALS in other groups of European ancestry.

A gloved hand holding a petri dish.

NIH Blueprint empowers drug development for nervous system disorders
Thursday, Aug 18, 2011
The NIH Blueprint for Neuroscience Research has made awards to investigators across the United States for an ambitious set of projects seeking to develop new drugs for disorders of the nervous system. The projects are part of the NIH Blueprint Neurotherapeutics Network, which will be funded at up to $50 million over the next five years.

A human astrocyte

New model of ALS is based on human cells from autopsied tissue
Thursday, Aug 11, 2011
By isolating cells from patients' spinal tissue within a few days after death, researchers funded by the National Institutes of Health have developed a new model of the paralyzing disease amyotrophic lateral sclerosis (ALS). They found that during the disease, cells called astrocytes become toxic to nerve cells – a result previously found in animal models but not in humans.

Motor neurons derived from human iPS cells

Induced Pluripotent Stem Cells Give Investigators a New Window into Neurological Disease
Friday, Jun 24, 2011
It is possible to take a sample of skin cells and induce them to behave like embryonic stem cells. Scientists are using these so-called induced pluripotent stem (iPS) cells to study disease mechanisms and test potential therapeutic drugs. In 2009, NINDS funded three consortia to develop iPS cell lines from individuals with Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and Huntington’s disease.

The structure of the normal SOD1 protein.  Image courtesy of Nature Neuroscience.

New Links Found between Familial and Sporadic ALS
Friday, Dec 17, 2010
After 1993, when mutations in the SOD1 protein were first connected to familial ALS, SOD1 became the most studied protein in ALS research. However, there have been doubts about SOD1's relevance to sporadic ALS (sALS). A new study in Nature Neuroscience shows that in people with sALS, it is possible to detect SOD1 protein that is genetically normal but has properties similar to mutant SOD1.

The neuromuscular junction of a healthy mouse looks similar to a bunch of grapes, and is shown in red and green thanks to the use of fluorescent antibodies.

MicroRNA Triggers Protective Response in Mice with ALS
Tuesday, Mar 2, 2010
In a recent study, investigators found that mice with amyotrophic lateral sclerosis (ALS) mount a protective, though ultimately unsuccessful, response against the disease. Central to this response is a small molecule called microRNA-206. Identifying ways to stimulate the molecule or its effects may lead to new treatments for ALS.

Four New Members Appointed to National Neurological Disorders and Stroke Advisory Council
Thursday, Feb 4, 2010
Four New Members Appointed to National Neurological Disorders and Stroke Advisory Council

Therapy Investigated for ALS May Find New Role in Kennedy’s Disease
Monday, Oct 26, 2009
A growth factor that has generated tides of hope and disappointment for treating amyotrophic lateral sclerosis (ALS) may turn out to be an effective therapy for a less common disease, Kennedy’s disease.

NINDS Names Dr. Petra Kaufmann Director of the Office of Clinical Research
Wednesday, Sep 9, 2009
The National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, has named Petra Kaufmann, M.D., M.Sc., as director of its Office of Clinical Research.

Image of motor neurons courtesy of Dr. George Mentis, NINDS.

Genetic Factor Extends Survival in People with ALS
Tuesday, Jun 16, 2009
Researchers funded in part by the National Institute of Neurological Disorders and Stroke (NINDS) have identified a gene that affects how long people survive with the fatal neurological disease amyotrophic lateral sclerosis (ALS). The finding could lead to much needed drugs to slow the course of the disease.

Support Cells Trigger Neuron Death in ALS
Thursday, Aug 2, 2007
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.

Large-Scale Gene Study Identifies Clues about Sporadic ALS
Tuesday, Apr 3, 2007
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.

Six New Members Named to National Neurology Advisory Council
Thursday, Oct 5, 2006
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.

Javits Neuroscience Award Presented to Six Leading Scientists
Wednesday, Jul 12, 2006
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.

Neurons Grown From Embryonic Stem Cells Restore Function In Paralyzed Rats
Tuesday, Jun 20, 2006
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).

NINDS Announces New Javits Neuroscience Investigator Awardees
Wednesday, May 4, 2005
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).

What's Old is New Again - Antibiotic Protects Nerves By Removing Excess Glutamate
Monday, Feb 7, 2005
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.

Study Using Robotic Microscope Shows How Mutant Huntington's Disease Protein Affects Neurons
Wednesday, Oct 13, 2004
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.
Fact Sheet

Study in Mice Links Growth Factor to Hereditary Motor Neuron Disease
Wednesday, Jul 7, 2004
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

Senataxin Gene Linked to Juvenile-Onset ALS
Wednesday, Jun 23, 2004
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

Misbehaving Molecules: 3-Dimensional Pictures of ALS Mutant Proteins Support Two Major Theories About How the Disease is Caused
Sunday, May 18, 2003
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

Transport Problems Cause Motor Neuron Degeneration
Thursday, May 1, 2003
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

Doubling Up: Researchers Combine a Common Dietary Supplement with an Antibiotic to Treat Lou Gehrig's Disease
Friday, Jan 31, 2003
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

Study Identifies Gene That Prevents Nerve Cell Death
Friday, Oct 25, 2002
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

Minocycline Delays Onset and Slows Progression of ALS in Mice
Thursday, May 2, 2002
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

NINDS Hails Advance in ALS Research
Wednesday, May 15, 1991
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.
Fact Sheet