Administered medications, cardiac monitoring and interpretations as well as performing intubations on
ALS patients
Not long ago, a clinical trial for
ALS patients discovered that microscopic changes in the spinal cord could be seen when the advanced MRI technique of diffusion tensor imaging was applied.
Therapeutics targeting microglia have slowed disease progression in rodent models, but have failed to translate into effective therapy for
ALS patients.
Now that we know that DM and ALS are related, we are studying ways to diagnose and measure disease progression with similar diagnostic modalities used in
ALS patients.»
The generosity It's Just Lunch has shown already and the continued support of its membership will help to speed that research and will provide hope to tens of thousands of
ALS patients all over the world.»
A staff of more than 25 scientists and technicians work on behalf of
ALS patients to discover and advance the best new ideas for stopping ALS.
«We are identifying these toxic, persistent, environmental pollutants in higher amounts in
ALS patients compared to those who do not have ALS,» said study co-author Dr. Stephen Goutman.
Scientists hope that by analyzing the genomes of larger numbers of
ALS patients, they will identify rare or subtle genetic changes that contribute to the disease.
Working with motor neurons derived from
ALS patients and healthy controls, Dr. Wainger performed fundamental electrophysiological characterization and identified motor neuron hyperexcitability in ALS patient - derived motor neurons (Wainger et al., 2014).
An international collaboration called Project MinE will use thousands of patient samples to hunt for rare genetic changes that distinguish
ALS patients from people without the disease.
In addition, three California - based ALS research labs have joined forces to form the Neuro Collaborative, which will create induced pluripotent stem (iPS) cell lines from
ALS patients that can be used to screen for new drugs and will be shared with the other groups.
Gladstone generated the model by transforming skin cells from
ALS patients into stem cells, known as induced pluripotent stem cells (iPS cells), and then programming them into neurons.
Mutations in genes underlying familial ALS (fALS) have been discovered in only 5 - 10 % of the total population of
ALS patients [5].
BMAA has been demonstrated to be concentrated in the brains of
ALS patients (but not controls) in Florida [19] and to be mis - incorporated into neuronal proteins via the L - serine tRNA - synthetase system [20 — 22].
Approximately 30,000 people in the United States live with the disease at any given time, while the global population of
ALS patients is approximately 400,000.
In addition to helping patients suffering from blood diseases, we are seeing advances in using stem cells to improve the condition of Alzheimer's, Parkinson's and
ALS patients everyday, and Dr. Maharaj is right there at the forefront of all of it.»
«We are optimistic about what the results of our joint efforts might mean to
ALS patients in the future,» added Dr. Finkbeiner, who is also a UCSF professor.
After a genetic mutation was discovered in a small group of
ALS patients, scientists transferred that gene to animals and began to search for drugs that might treat those animals.
ALS patients show progressive muscle weakness and atrophy, leading to a...
Thus, that study results arguably applies to
ALS patients as well.
Neurons, red, created from
ALS patients bearing the C9orf72 mutation, show clumps of the RanGAP protein, yellow, in their nuclei, white.
This causes
ALS patients to progressively lose muscle mass, resulting in loss of strength in the limbs and problems with speaking, swallowing, and breathing.
Ten percent of
ALS patients suffer from a familial form of the disease, while FTD is caused in 40 % of patients by a genetic defect.
We also found that in families with both FTD and
ALS patients, if the parent had FTD the child was more likely to have FTD, and a similar principle applied to ALS.»
For
ALS patients like Gilmore, the research can't come soon enough.
Thus, that study results arguably apply to
ALS patients as well.
New England's ALS hot spots In New Hampshire, Dartmouth neurologist Elijah Stommel noticed that several
ALS patients came from the small town of Enfield in the central part of the state.
TDP - 43 is a protein that misfolds and accumulates in the motor areas of the brains of
ALS patients.
In further studies, the researchers found that TIA1 mutations occurred frequently in
ALS patients.
Watching how stem cells (derived from
ALS patients» own skin cells, for example) develop into motor neurons will offer new insights into disease processes, and any method that improves the speed and efficiency of generating the motor neurons will aid scientists.
The two
ALS patients achieved 2.2 and 1.4 bits per second, respectively, more than doubling previous records (held by these same participants in a previous study from this group).
These speeds also approach what
ALS patients questioned in a survey said they would want from a BCI device.
A team led by scientists at St. Jude Children's Research Hospital and Mayo Clinic has identified a basic biological mechanism that kills neurons in amyotrophic lateral sclerosis (ALS) and in a related genetic disorder, frontotemporal dementia (FTD), found in
some ALS patients.
«Study uncovers key differences among
ALS patients.»
«Last year, the ALS Ice Bucket Challenge raised a remarkable amount of money to support
ALS patients and research,» Dr. Petrucelli says.
The researchers also discovered that c9RAN proteins produced by the abnormal RNA can be measured in the spinal fluid of
ALS patients.
Their findings, reported online in Nature Neuroscience, demonstrate that
ALS patients show abnormalities in levels and processing of ribonucleic acids (RNA), biological molecules that determine what gene information is used to guide protein synthesis.
ALS patients show progressive muscle weakness and atrophy, leading to a fatal respiratory muscle paralysis.
These results provide us with new perspectives regarding future therapeutics, especially focused on preventing the MAM disruption for
ALS patients.
A decade ago, they also identified a relationship between ALS and excess iron accumulation when they found that 30 percent of
ALS patients in their clinic carried a variant of a gene known as HFE that is associated with iron overload disease.
Mice bred to carry a gene variant found in a third of
ALS patients have a faster disease progression and die sooner than mice with the standard genetic model of the disease, according to Penn State College of Medicine researchers.
Understanding the molecular pathway of this accelerated model could lead to more successful drug trials for
all ALS patients.
That is good news for
ALS patients seeking better treatment options.
The antibiotic minocycline seemed to be a promising treatment for ALS in mice, so why was it so hard to recruit
ALS patients for a human trial?
Brown cautions that the presence of the defective gene will need to be confirmed in many more
ALS patients.
There are some 30,000
ALS patients in the United States alone.
They also tested samples from 13
ALS patients, all of which tested positive for BMAA.
Then, a couple of years ago, in an effort to gain more insight into the disease, Stommel enlisted students to punch the street addresses of about 200 of
his ALS patients into Google Earth.
He and Cox are conducting tests of brain bank tissue to see if
the ALS patients in these regions do in fact have elevated levels of BMAA.
The researchers found that
the ALS patients» neurons worked very similarly to the preclinical research findings.