Articles tagged with Amyotrophic Lateral Sclerosis
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Researchers have identified three new risk genes for amyotrophic lateral sclerosis (ALS) using genetic data from Project MinE. One of these genes, C21orf2, increases the risk of developing ALS by 65%. The study's findings could aid the development of personalized treatments using gene therapy.
Scientists from the University of Sheffield have discovered a novel function of the C9orf72 protein, which is linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The study found that the C9orf72 protein regulates the initiation of autophagy, a vital process for nerve cell survival.
Researchers found that transplanting human stem cells into the spinal cord was done safely, but did not slow down the progression of the disease. The treatment resulted in temporary side effects, including pain and swelling, but no conclusive evidence of effectiveness was found.
Researchers have found that measuring copper and zinc concentrations in blood and tissue may allow for early diagnosis of Amyotrophic Lateral Sclerosis (ALS). The study, presented at the Goldschmidt conference, showed significant changes in these elements prior to symptom onset.
Researchers at Umeå University have discovered that aggregated SOD1 protein in motor neurons causes rapid spread of ALS in mice. The study suggests a domino effect that spreads the disease up the spinal cord, mirroring human cases with hereditary traits for ALS.
Researchers created a mouse model that closely replicates the symptoms and gene expression patterns of ALS and frontotemporal dementia. The model allows scientists to understand how the C9orf72 gene mutation causes paralysis and dementia, and potentially develop treatments.
Lauren Sciences will use the grant to customize LAUR-301 with neurotrophic factor and deliver it to disease sites in central nervous system ALS mice. The company aims for LAUR-301 to enter human clinical trials and become a transformative V-Smart TM Nanomedicine for treating ALS.
Researchers at Oregon State University have developed a therapy that halts the progression of ALS in mice for nearly two years, allowing them to approach their normal lifespan. The treatment uses copper-ATSM, which delivers copper specifically to cells with damaged mitochondria and has low toxicity.
A team of researchers discovered a protein called Pur-alpha that can protect against toxic degeneration in cells, which may lead to a treatment for ALS. The study suggests that Pur-alpha could serve as a novel therapeutic target for developing a treatment for ALS patients.
Matthew D. Disney's innovative approach uses cells as reaction vessels to synthesize treatments within disease-affected cells, offering highly specific and precise therapies. This technology has potential applications in treating over 30 incurable diseases, including ALS, fragile X syndrome, and Huntington's disease.
Researchers at Barrow Neurological Institute and TGen will analyze blood and CSF samples from 60 participants to identify peptide, protein, and RNA biomarkers indicative of ALS progression. The goal is to develop effective treatments for patients in clinical trials.
Researchers found that the most common genetic defect in ALS causes nuclear pore dysfunction, leading to cell death. This discovery empowers the search for genetic causes of sporadic ALS and offers new hope for treatment options.
Researchers developed a fly model to study age-dependent neurodegeneration at single cell resolution, identifying three genes involved in the process. The findings have relevance for understanding ALS progression and could lead to therapies for neurodegenerative diseases.
Researchers found that groups of neurons work together to signal muscles about when and where to move, firing in complex rhythms. The study aims to create prosthetic devices that better understand and respond to a person's thoughts.
Scientists at the University of Montreal have discovered a new approach to treating amyotrophic lateral sclerosis (ALS) by targeting the immune system. The study, published in Nature Communications, found that an imbalance of the immune system can contribute to ALS and trigger motor neuron destruction.
Researchers at the University of Toronto have identified a possible way to predict if an individual is genetically prone to ALS by analyzing DNA repeats in the C9orf72 gene. The study found that a certain number of repeats, when modified with methyl groups, can cause the disease.
Researchers at Mayo Clinic developed a mouse model exhibiting neuropathological and behavioral features associated with C9ORF72 mutation. The study suggests a link between the repeat expansion in C9ORF72 and TDP-43 pathology, potentially leading to therapeutic agents targeting RNA foci and c9RAN proteins.
Hristelina S. Llieva will receive a two-year Clinical Research Training Fellowship in ALS to investigate glial cell dysfunction contributing to familial ALS. The award supports her work on the C9ORF72 linked subtype of familial ALS, which is viewed as a predominantly neuronal disease.
Scientists have found that senataxin, a protein associated with neurodegenerative diseases, plays a key role in the body's natural antiviral response. Abnormal inflammation generated by senataxin deficiency may contribute to disease progression in conditions like ALS.
A recent study has identified a group of gene variants that may contribute to sporadic motor neurone disease, a devastating condition affecting thousands of Australians. Researchers sequenced the protein-coding genes of 44 MND-affected individuals and their parents, finding rare genetic changes in two-fifths of cases.
Researchers have identified a new gene, TBK1, associated with sporadic ALS, highlighting the importance of inflammation and autophagy pathways. The study also found that OPTN may be a major player in the disease, interacting physically and functionally with TBK1.
Researchers found 26% of sporadic ALS patients carry potential mutations in known ALS genes, suggesting genetic errors contribute to significantly more cases. Mutations in multiple genes can accelerate disease onset.
Researchers found that blocking the ALS mutation in the brain slowed disease onset and progression, suggesting that early dysfunction of brain motor neurons may contribute to later disease development. The study used rats with ALS, showing delayed disease onset and extended survival when suppressing the mutation in the brain.
Researchers found that aging astrocytes lose ability to protect motor neurons, but replacing old cells with engineered protein improves neuron survival. A specially engineered protein called GDNF increases motor neuron survival when cultured with aging astrocytes.
Researchers identified the TUBA4A gene as associated with familial amyotrophic lateral sclerosis (ALS), a fatal neurological disorder. The mutated protein weakens the microtubule network, leading to motor neuron death and paralysis.
A new study suggests that ALS progression is linked to increased protein instability, particularly in mutant superoxide dismutase (SOD) proteins. The researchers found that SOD clusters or aggregates are common in affected motor neurons and support cells, suggesting a potential target for therapy.
Rabies uses a nerve growth factor receptor to enter the central nervous system, where it causes acute inflammation and violent aggression. The virus manipulates neuronal transport machinery to move faster than normal, allowing it to reach the brain with maximum speed.
The team determined the high-resolution structure of Dbr1 enzyme, which breaks loops of ribonucleic acids and could be a new target for treating most cases of ALS. By inhibiting this enzyme's activity, researchers hope to prevent TDP-43 aggregates from forming in motor neurons.
The ALS Association granted Lauren Sciences LLC a grant to develop a V-Smart therapeutic for amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease. The project aims to deliver neurotrophic factors across the blood brain barrier using the company's novel V-Smart nanovesicle platform technology.
Researchers found that serum albumin and creatinine levels are related to ALS survival in both sexes. Lower albumin and creatinine levels are related to worse clinical function at diagnosis.
Researchers found a significant association between higher dietary intakes of total ω-3 PUFAs and reduced risk for ALS. Consuming both α-linolenic acid (ALA) from plant sources and marine ω-3 PUFAs contributed to this protective effect, while ω-6 PUFA intake was not linked to ALS risk.
Researchers have found that boosting autophagy, a cell-cleaning process, can help clear abnormal protein buildup in brain cells. Three drugs that enhance autophagy showed promise in keeping brain cells alive longer, potentially offering new treatment options for conditions like ALS and dementia.
Researchers found over-activity of enzyme HDAC6 exacerbates ALS symptoms in fruit-flies, highlighting potential therapeutic avenues. Inhibition of HDAC6 may offer protective effects against the disease.
Researchers at Oregon State University have discovered a copper compound that significantly extends the lifespan and improves locomotor function of transgenic mice with ALS. By delivering copper selectively to spinal cord cells, scientists aim to stabilize superoxide dismutase and improve mitochondrial function.
Researchers at the University of Calgary have found a way to promote growth in damaged nerve cells by inactivating protein Rb, which normally acts as a brake on nerve growth. This discovery has the potential to treat conditions such as peripheral nerve disorders, including diabetic neuropathy and multiple sclerosis.
A University of Wisconsin-Madison researcher has pinpointed an error in protein formation that could be the root of amyotrophic lateral sclerosis. Motor neurons that control foot muscles are affected due to a shortage of one of three proteins in neurofilaments, leading to tangles and nerve fiber malfunction.
Researchers aim to deliver GDNF into muscle cells using a viral vector to protect motor neurons and slow disease progression in a rat model of ALS. The study, led by Cedars-Sinai Regenerative Medicine Institute, could pave the way for a clinical trial if successful.
Researchers at USC have found that an experimental drug protects the blood-spinal cord barrier's integrity in mice with ALS, delaying motor neuron degeneration and potentially offering new hope for treatment. The study suggests that repairing damage to the blood-spinal cord barrier may delay disease progression in people with ALS.
A study led by University of British Columbia researchers reveals how the fatal neurodegenerative disease ALS is transmitted from cell to cell. The research shows that misfolded non-mutant SOD1 can be transmitted regionally in the nervous system, offering a molecular explanation for ALS progression.
Researchers at St. Jude Children's Research Hospital found that ALS-causing mutations disrupt RNA transport in nerve cells, leading to protein misassembly and cell death. The study provides a new focus for treating ALS, a neurodegenerative disease associated with muscle weakness and paralysis.
Researchers identified two genetic variations in the MAPT gene associated with sporadic amyotrophic lateral sclerosis (ALS) in the Chinese Han population. Patients with these variations were more prone to bulbar palsy and breathing difficulties than those with the wild-type genotype.
Researchers from the University of Pennsylvania have discovered a way to reduce disease toxicity associated with Lou Gehrig's disease in animal models. By targeting stress granules and modulating cellular structures, they slowed neuron dysfunction and showed promise in mammalian cells.
Joost van der Westhuizen, a former World Cup-winning rugby star, is partnering with the University of Edinburgh's Euan MacDonald Centre for Motor Neurone Disease Research to raise awareness and funds. The collaboration aims to share knowledge and expertise to benefit MND patients.
A team of doctors and scientists at Cedars-Sinai Medical Center used stem cell technology to create neurons from patients' skin cells and block the damaging effects of a defective gene. The study provides proof of concept for a new therapeutic strategy, suggesting a potential future therapy for Lou Gehrig's disease.
Kaiser Permanente's Complete Care model has shown steady improvement in quality scores, with an average increase of 13% compared to the national average. The program uses Proactive Office Encounters to address patient needs, promoting preventive care and improving chronic condition management.
Researchers from the University of Sheffield and Mario Negri Institute in Italy investigated two mouse models of MND, identifying key differences in gene expression that may help predict disease duration. The study provides new insights into mechanisms that slow down disease progression.
University of Adelaide researchers have identified a likely molecular pathway that causes neurodegenerative diseases such as Huntington's and Lou Gehrig's. The team found that RNA plays a key role in the development of these diseases, which share similar genetic mutation mechanisms.
Researchers developed a staging system to track ALS disease progression, mapping out four distinct stages and identifying transmission patterns. The study's findings suggest a similar transmission process in other neurodegenerative diseases, such as Alzheimer's and Parkinson's, and may lead to new treatments like immunotherapies.
Researchers at Stanford University School of Medicine have identified mutations in genes that encode chromatin regulators, which may contribute to the development of sporadic ALS. The study found 25 de novo mutations, including five in chromatin regulatory proteins, which could serve as potential therapeutic targets.
Researchers at Northwestern University have isolated and labeled motor neurons in the brain that die in ALS, allowing for the study of disease progression. The discovery paves the way for identifying potential treatments for the devastating neurodegenerative disease.
Researchers at the University of Pittsburgh School of Medicine found that melatonin injections delayed symptom onset and reduced mortality in a mouse model of ALS. The study suggests that melatonin may be a useful treatment for this devastating disease.
Researchers discovered a novel compound that promotes motor neuron survival, offering a new approach to treating ALS. The study used stem-cell-derived motor neurons and screened over 5,000 compounds, finding kenpaullone to be more effective than existing treatments.
Scientists aim to unravel the mystery of microtubule directional signs, crucial for understanding diseases like Alzheimer's and ALS. The study's focus is on identifying modifications that could serve as road signs along molecular highways.
Researchers at Mayo Clinic discovered an abnormal protein C9RANT that accumulates in the brains of patients with ALS and frontotemporal dementia. The findings provide a potentially new therapeutic target and biomarker to confirm diagnosis of these diseases.
Researchers created motor neurons and astrocytes from a patient's skin cells, revealing that abnormal TDP-43 protein causes astrocyte death. This finding provides fresh insight into the mechanisms of motor neurone disease, a devastating condition with no cure or effective treatment.
Researchers have identified a new genetic mutation in the ARHGEF28 gene that is present in all cases of amyotrophic lateral sclerosis (ALS). The protein arising from this gene appears to play a critical role in the disease, and understanding its function could lead to targeted therapies.
Researchers found that stem cell transplantation significantly extended the lifespan of mice with ALS by 20 days and improved their neuromuscular function by 15 percent. This breakthrough study suggests that stem cells may represent a promising avenue for effective cell-based treatment for ALS and other neurodegenerative diseases.
Researchers have shown that transplanted neural stem cells slow ALS onset and progression, improving motor function and survival time. The study also found that these cells promote the production of protective molecules and reduce inflammation.
A new study by LSUHSC researchers has found that the ability of a protein called FUS to bind to RNA is essential to the development of Amyotrophic Lateral Sclerosis (ALS). By mutating FUS and blocking its RNA binding, the team was able to suppress ALS-related neurodegeneration in fruit fly models.
In a groundbreaking study, researchers found that transplanted neural stem cells slow ALS disease onset and progression by producing protective molecules and reducing inflammation. The treatment improves motor function and prolongs survival in ALS mice, offering new hope for treating this devastating disease.