Articles tagged with Amyotrophic Lateral Sclerosis
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A new study identified Gemin3 as a molecular 'bridge' between genes causing amyotrophic lateral sclerosis (ALS), a neurodegenerative disease. The research holds promise for developing treatments effective for a broad range of ALS patients.
Researchers at KBRI found a new molecular mechanism that can inhibit neuronal degeneration by TDP-43, which is a major cause of dementia and Lou Gehrig's disease. The discovery reveals a potential therapeutic strategy to remove abnormal protein accumulation in neurons of patients with dementia.
A recent study by Cold Spring Harbor Laboratory has made significant strides in understanding the role of proteins called TDP-43 in ALS. The researchers found that TDP-43 aggregates in nerve cells can cause a toxic effect, leading to paralysis. This discovery opens up new avenues for developing effective treatments and therapies.
Researchers found that ALS patients with a specific genetic variation in the IL6 receptor gene experience more severe symptoms and faster disease progression. The study suggests this polymorphism may serve as a target for new treatments and lay the groundwork for future clinical trials.
Researchers at Neuroscience 2019 announce new gene therapy research promising to prevent, treat, and reverse incurable neurological disorders. Successes in restoring lost functions in animal models of neurological diseases are discussed, as well as technique advancements that may improve future treatments.
Amyotrophic Lateral Sclerosis (ALS) researchers found that aggregation of TDP-43 is not harmful but actually protects cells. This discovery challenges the assumption that alleviating protein aggregates is necessary to treat neurodegenerative diseases like ALS. The study opens doors to radically new therapeutic approaches if aggregation...
Researchers at Oregon State University have made an important advance in understanding why certain cells in the nervous system are prone to breaking down and dying, which is what happens in patients with ALS. The study suggests that a protein chaperone called heat shock protein 90 may be critical to neuron survival.
Scientists at MSD and Francis Crick Institute are working together to better understand Motor Neurone Disease, a devastating disease with no current treatments. The collaboration aims to identify key mechanisms that can kill motor neurons and build scientific understanding for future treatments.
Northwestern University scientists have received a $3.1 million grant to investigate drug therapies for ALS, targeting protein aggregation and upper motor neurons. Promising early results suggest compounds may have broader applications for neurodegeneration.
Researchers found that protein clumps in ALS neurons can be triggered by cellular stress and may provide a potential target for new therapies. Chemical compounds have been identified to prevent this stress-induced accumulation, offering a promising starting point for treating the disease.
Increasing Klotho levels improves neurological deficits and prolongs life span in an experimental ALS model. Brain immune cells also play a crucial role in protecting the brain against inflammation and motor neuron loss.
A $2.88 million NIH grant supports Jingsong Zhou's work to preserve mitochondria and understand the mechanisms behind ALS deterioration. Her novel approach investigates the theory that ALS affects the physiology of the whole body through defective cells in multiple organs.
Researchers found a critical structure within TDP-43 that causes nerve cell death in ALS and FTD. Modifying this structure could lead to new therapies for these devastating diseases.
Researchers found that the most common genetic cause of ALS, C9orf72 mutation, leads to toxic dipeptide repeat polypeptides (DPRs) disrupting nucleolar assembly. Longer DPRs are more toxic to cells, highlighting a potential prognostic value for ALS patients.
St. Jude scientists discover that ULK1 and ULK2 break down stress granules, which build up toxic proteins that kill muscle and brain cells in diseases including IBM, ALS, and FTD. Boosting these enzymes could help treat the conditions.
Lauren Sciences LLC has received an AU$1 million grant from FightMND to advance its development of LAUR-301, a novel V-Smart Nanomedicine for ALS. The therapy aims to protect motor neurons and induce neuro-restoration, slowing or reversing the disease.
Researchers developed an antibody to target TDP-43 protein aggregates in mouse brains, resulting in significant improvements in cognitive and motor performance. The breakthrough paves the way for immunotherapy development for ALS and frontotemporal dementias.
Researchers have developed a rodent model that mimics human swallowing problems in ALS, allowing for targeted study of preserving and restoring swallowing function. The research could one day lead to new treatments to slow the disease and improve quality of life for individuals with ALS.
A team of researchers from North Carolina State University has identified two promising proteins, chitinase-3 like1 and alpha-1-antichymotrypsin, that may improve the diagnosis and prognosis of ALS. The study found that models developed from proteins in cerebrospinal fluid were more useful than those in blood plasma.
Houston Methodist researchers have identified a repair defect in nerve cells that sends messages to the brain, potentially leading to a therapy for preventing or slowing down ALS. The team discovered a DNA Ligase-targeted therapy could inhibit oxidative damage repair in Amyotrophic Lateral Sclerosis.
A University of Bath team has biochemically characterised the protein produced by the C9orf72 gene, revealing it to be a guanine nucleotide exchange factor (GEF) that regulates molecules called RABs. This understanding is crucial in developing treatments and potentially a cure for neurodegenerative diseases ALS and FTD.
Researchers used muscle-on-a-chip technology to model ALS, revealing a promising treatment combination that may improve symptoms. The study found that combining two neuroprotective molecules can efficiently cross the blood-brain barrier and recover muscle contraction and neuronal survival.
A new study published in Neurology shows that amyotrophic lateral sclerosis (ALS) affects the mind, especially later in the disease, leading to cognitive and behavioral problems such as apathy, changes in eating behaviors, and loss of sympathy or empathy. People with ALS are recommended to be routinely screened for these issues.
Researchers developed a new method to measure degeneration of sensory neurons grown in a lab, improving the screening of experimental therapies for neurodegenerative diseases. The automated test uses software-assisted analysis to accurately assess nerve cell densities and shapes.
Researchers at Penn Medicine discovered PARP inhibitors could prevent toxic TDP-43 accumulations in brain cells. The treatment shows promise for neurodegenerative disorders like ALS and FTD.
Researchers found that supplementing mitofusion 2 protein could prevent nerve degeneration, muscle atrophy, and paralysis in a mouse model of Lou Gehrig's disease. The study suggests this approach may be a novel therapeutic strategy for the disease.
Researchers discovered that Kapβ2, a nuclear localization signal, plays a crucial role in transporting the FUS protein into the nucleus. The study found that when this system fails, FUS proteins aggregate and form toxic droplets, contributing to neurodegenerative diseases like familial ALS.
Researchers found that infusions of properly functioning Tregs significantly slowed ALS disease progression in patients. The treatment increased Treg levels by 30-40% and showed promise as a potential treatment for the debilitating disease.
A recent study published in Nature Communications has found that ebselen can correct many of the toxic characteristics of a protein causing some cases of hereditary motor neurone disease (MND). The drug-molecule can restore important steps in the SOD1 assembly process, potentially preventing neuronal cell death.
The ALS Association granted Lauren Sciences LLC its third award for developing LAUR-301, a V-Smart Nanomedicine for ALS. LAUR-301 aims to deliver GDNF across the blood-brain barrier and induce neuro-restoration in all ALS patients.
An international team has confirmed a new genetic mutation link to amyotrophic lateral sclerosis (ALS) by identifying KIF5A as a key player in axonal transport. The study used massive amounts of genetic data to pinpoint the link, providing important new directions for future gene therapies.
Timothy M. Miller receives award for work on effective therapies for ALS, developing method to turn off toxic protein production in brain and spinal fluid. His approach is currently being tested in human clinical trials.
Researchers at Syracuse University are making progress in understanding the disease mechanism of ALS by studying ubiquitin and Ubiquilin-2 protein interactions. They found that ubiquitin eliminates droplets of UBQLN2, a protein-encoding gene linked to ALS and dementia.
Changes in neuron size have been linked to the progression of motor neurone disease, with vulnerable neurons increasing in size before symptoms appear. This could lead to new strategies for slowing or halting nerve cell death and improving treatment options.
Researchers studied angiogenin's entry into central nervous system cells to better understand its role in brain diseases like ALS and dementia. The study found that angiogenin uptake has multiple biochemical pathways, revealing a more intricate mechanism than initially thought.
A study suggests that frequent exposure to diesel exhaust may increase the risk of amyotrophic lateral sclerosis (ALS), with a stronger link observed in men exposed for more than 50% of their working life. The research, published in the American Academy of Neurology's meeting program, found no associations among women, highlighting the...
Researchers at USC discovered a cellular mechanism that limits the number of 'cellular janitors' in the nervous system, leading to increased risk for ALS and frontotemporal dementia. The study found that a mutation in the C9ORF72 gene causes toxicity in nerve cells, resulting in cell death and degeneration.
Researchers at Western University have discovered a unique neurobiological pathway triggered by head trauma that underlies both Chronic Traumatic Encephalopathy (CTE) and Lou Gehrig's disease. The study, published in the January 2018 issue of Neurology, identifies a common link between CTE and ALS-related cognitive impairment.
Researchers at Hokkaido University have shed light on the molecular mechanisms behind ALS by studying the depletion of protein TDP-43. The study found that TDP-43 binds to U6 snRNA, stabilizing it, which leads to its degradation and eventual cell death. This discovery may lead to ways to slow or stop neuronal cell death in ALS patients.
A study published in Nature Communications reveals a genetic mutation in the C9orf72 gene causes a vicious cycle of toxic protein production, driving neuronal death in ALS. The researchers found that cell stress activates more toxic protein production, creating a loop that potentially drives disease progression.
Researchers have identified multiple misfolded pathways and intermediate states in the protein superoxide dismutase-1 (SOD1), a key player in ALS. Understanding these pathways is crucial for developing targeted therapeutic interventions.
Researchers studied 3000 human neuromuscular junctions, revealing details of their anatomy and structure. Human NMJs were found to be smaller and frailer than those in mice and rats, with no effect of age on their health.
Researchers discovered a new mechanism to prevent RNA from leaving cells' nuclei, leading to fresh treatment approaches for the most common form of motor neurone disease. By targeting SRSF1 protein, it's possible to reduce rogue RNA molecules and open up new areas of investigation for gene therapy.
A study published in Neurology found that approximately 17% of ALS cases are caused by gene mutations, with rare and likely harmful variants being more common in those with the disease. The research highlights the importance of genetic factors in ALS development and suggests a larger percentage of sporadic cases may be linked to genetics.
A new study has found that a decades-old malaria drug can safely lower levels of a toxic protein linked to familial ALS. The research suggests the drug could potentially slow disease progression in patients with genetic mutations.
A molecule called polyGP accumulates in the CSF and blood cells of patients with C9ORF72 ALS, offering a potential pharmacodynamic marker for therapeutic responses. Detection of polyGP in asymptomatic carriers may help identify patients at risk before symptoms appear.
Research published in Occupational & Environmental Medicine found a doubling of ALS risk among men exposed to very low frequency electromagnetic fields at work. High levels of exposure were associated with nearly twice the likelihood of developing the disease.
A new study suggests that consuming fish and seafood with higher levels of mercury may increase the risk of amyotrophic lateral sclerosis (ALS). The study found that individuals who ate fish and seafood regularly were at double the risk for ALS compared to those with lower mercury intake.
Researchers found that children of parents with C9orf72 mutations are more likely to develop frontotemporal dementia and ALS at a younger age, without accelerated disease progression. The study suggests that the length of the C9orf72 repeat is determinative for the age of onset of the disease.
A team of biomedical scientists has identified a molecule that targets the EphA4 receptor, a gene associated with rapid ALS progression. The research aims to delay motor neuron death and explore potential applications in spinal cord injury, Alzheimer's disease, and some cancers.
Researchers at the University of Illinois College of Medicine found that butyrate corrected a gut microbiome imbalance and reduced gut leakiness in mice with ALS. The treated mice lived longer than control mice and showed improved neuromuscular function.
A naturally occurring growth factor called FGFBP1 is secreted by muscle fibers to maintain neuromuscular junctions. However, ALS patients have reduced levels of FGFBP1 due to the accumulation of TGF-beta, a growth factor associated with the immune system.
Researchers have developed a groundbreaking 3D imaging technique that maps the reorganization of genetic material in cell nuclei, providing a new understanding of how chromosomes are compacted and genes are activated or silenced. This breakthrough uses X-ray microscopy to visualize the structure and movement of chromatin in real-time.
The study found that the GSK3 enzyme regulates the persistent sodium current, which affects a nerve cell's excitability and firing activity. This discovery may lead to chronotherapeutics, where treatments are tailored to the time of day to maximize health benefits and minimize side effects.
Researchers have developed two new mouse models of amyotrophic lateral sclerosis (ALS) that exhibit protein clumping and display clinical features seen in patients. The models may help scientists better understand the disease and develop new treatments.
High physical fitness increases ALS risk before age 45, while individuals with high IQs have increased risk at 56+ years. Individuals with lower BMI (25+) show reduced risk across all ages.
A new study found that antioxidant nutrients, fruits, and vegetable intake are associated with better ALS function at baseline. The analysis of 302 ALS patients suggested promoting fruit and vegetable intake to support nutritional care.
A major new study aims to uncover the secrets of ALS through research in Latin America, examining if mixed ancestry has a protective effect on developing the disease. The project will establish registers of incidence, prevalence, and risk factors for ALS in Cuba, Chile, and Uruguay.
Researchers discovered that RIPK1 damages neuronal axons by disrupting myelin production, leading to axonal degeneration and hallmark ALS symptoms. The findings suggest that inhibiting RIPK1 activity may halt the progression of ALS and provide new therapeutic options.
A groundbreaking study found that keeping a specific RNA binding protein, TDP-43, from moving inside nerve cells can prevent cell death and disease progression in ALS and other neurodegenerative disorders. The researchers developed small proteins to block the protein's localization, preventing toxicity and disease progression in mice.