Articles tagged with Amyotrophic Lateral Sclerosis
Research finds that leaky blood vessels in mice with ALS mutations expose neurons to toxic substances, contributing to disease progression. The study opens a new front in understanding ALS, a debilitating disease that affects motor neurons.
A team of Canadian and French researchers has identified the TDP-43 gene as a significant cause of ALS (sporadic amyotrophic lateral sclerosis), a neuromuscular disorder affecting motor neurons. The study, published in Nature Genetics, found that up to five percent of ALS patients have genetic mutations in this gene.
Researchers have identified a mutation in the TDP-43 gene linked to inherited amyotrophic lateral sclerosis (ALS) and suggest it may also play a role in common dementia. The study's findings could provide new insights into understanding ALS and developing treatments.
In a breakthrough study, targeting astrocytes in mice with amyotrophic lateral sclerosis (ALS) doubles the lifespan of affected animals. This finding suggests that astrocytes, support cells essential for neuronal function, may be viable targets to slow disease progression and extend life expectancy.
A study published in PLOS ONE found that mice with amyotrophic lateral sclerosis (ALS) have a compromised blood-spinal cord barrier, leading to vascular leakage and potential mechanisms for motor neuron damage. Researchers hope this finding will lead to the development of new treatments targeting the barrier's repair.
Researchers have found that mutated forms of the angiogenin gene are toxic to motor neurons and affect their ability to grow and extend. Targeting these faulty molecules may help maintain healthy neurons and prevent disease progression.
Scientists found that inhibiting Nox1 and Nox2 genes can slow down ALS progression in mice, leading to improved survival rates. The study suggests developing drugs targeting the Nox pathway could be beneficial for individuals with ALS.
Motor neurone disease is a degenerative disorder that causes loss of basic motor functions, with symptoms including bulbar-onset, cervical-onset, and lumbar-onset patients. The disease has been reported in certain populations, such as the Chamorro population on Guam, and may be linked to genetic and environmental factors.
Researchers at Johns Hopkins have shown that transplanting human stem cells into spinal cords of rats bred to duplicate Lou Gehrig's disease delays the start of nerve cell damage typical of the disease and slightly prolongs life. The transplanted stem cells develop into nerve cells that make substantial connections with existing nerves.
A new study reveals a common pathological process between frontotemporal dementia and amyotrophic lateral sclerosis (ALS), with misfolded protein TDP-43 identified as a key component. This discovery may lead to a better understanding of these devastating neurological diseases.
Researchers at Oregon State University have developed a new technique to visualize and measure superoxide in animal cells, offering a breakthrough in understanding degenerative diseases such as Lou Gehrig's Disease, heart disease, diabetes, and aging. The discovery could significantly speed up research on these conditions.
Researchers develop a novel approach to treat amyotrophic lateral sclerosis (ALS) by delivering an antisense oligonucleotide drug directly to the brain and spinal cord. The treatment slows disease progression by silencing mutant proteins that cause the disease, offering new hope for patients.
Researchers delivered antisense oligonucleotides through cerebrospinal fluid to treat neurodegenerative diseases like ALS. The therapy effectively modulated protein levels and slowed disease progression in rats.
Researchers found strong association between PON2-PON3 gene cluster polymorphisms and sporadic ALS, a complex neurodegenerative disorder. Gene variations may help elucidate the cause of sporadic ALS, potentially leading to specific treatments.
Researchers found that a high-caloric ketogenic diet slowed ALS progression in mice by promoting mitochondrial energy production and membrane stabilization. The study suggests that dietary interventions may offer new therapeutic options for ALS patients.
U of MN researchers identified the specific mutation causing Spinocerebellar ataxia type 5 (SCA5), a dominant gene disorder. The discovery enables genetic testing for patients at risk, providing improved diagnoses and insight into neurodegenerative diseases.
The study found that T cells recognize brain proteins and recruit resident immune cells to fight off toxic substances, enabling neurogenic regions like the hippocampus to form new nerve cells. This process is linked to local immune activity and may play a role in maintaining learning and memory abilities in adulthood.
A new way to stimulate the brain to release antioxidants has been discovered by researchers, potentially treating ischemic stroke, multiple sclerosis, and neurodegenerative disorders. The NEPPs compound activates the Keap1/Nrf2 pathway to regulate antioxidant production, offering a promising approach for neuroprotection.
Researchers found that exercise combined with gene therapy significantly extended the lifespan of mice with ALS, averaging 210 days, compared to 120 days in untreated mice. Early exercise initiation also improved outcomes, suggesting a potential strategy for slowing disease progression.
The Squid Genome Project aims to identify genes in squid that are essential for understanding debilitating neurological diseases. Researchers hope that this information will aid in the development of new treatments and therapies.
The AAN Foundation and ALS Association are partnering to provide funding for a Clinician Scientist Development Award in support of ALS research. The award aims to prioritize promising compounds for clinical trials, bringing hope to patients suffering from this debilitating disease.
Researchers found that riluzole, a glutamate modulating agent, reduced symptoms in 35% of patients with OCD. The study suggests that riluzole may represent a novel treatment intervention for certain anxiety and mood disorders.
Researchers at Johns Hopkins Medicine have identified two proteins that help replace calcium-allowing channels with ones that keep calcium out, potentially protecting nerve cells from Lou Gehrig's disease. The discovery may lead to new ways to harness the channel-changing ability in other brain cells.
Researchers have found that 47% of ALS patients exhibit reverse transcriptase activity, suggesting a potential link to retroviruses. Further study is needed to determine if this reflects activation of an endogenous retrovirus or infection with a novel exogenous retrovirus.
A recent study published in Neurology found no significant association between increased physical activity and the risk of developing amyotrophic lateral sclerosis (ALS). However, it was discovered that higher leisure time physical activities before age 25 resulted in an earlier onset of the disease by seven years.
A large multi-center clinical trial is planned to test the safety and efficacy of antibiotics in treating ALS. Daily injections of ceftriaxone delayed nerve damage and extended survival by 10 days in mice with a Lou Gehrig's disease model.
Researchers transplanted adult olfactory bulb stem cells into genetically engineered mice with ALS, showing a significant delay in disease symptoms and improved functional outcomes. The study suggests these stem cells may hold potential for treating ALS, but further laboratory work is needed.
Researchers have used human spinal cord cells to delay ALS symptoms in rats by 11 days. The study's findings suggest that neuronal stem cells may hold promise for treating conditions caused by separation within the nervous system.
Scientists have found that a longevity protein called SIRT1 delays the breakdown of axons in nerve cells, potentially slowing neurodegenerative diseases. The discovery opens new avenues for treating Parkinson's disease, Alzheimer's disease, and other disorders.
Mitochondrial damage is a key factor in Lou Gehrig's disease, causing cells to die. The study reveals that mutant SOD1 protein clogs the transport system of mitochondria in muscle-controlling nerve cells.
Researchers have discovered biomarkers for ALS in cerebrospinal fluid, which could enable rapid diagnosis and prompt treatment. These biomarkers have high sensitivity and specificity, and may be used to monitor drug effectiveness in clinical trials.
A new gene mutation has been discovered for a rare form of inherited paralysis called hereditary spastic paraplegia. This breakthrough could lead to improved diagnosis and potential treatments for the condition, which affects around 20,000 Americans.
A study published in Neurology reveals that Gulf War veterans under 45 have developed ALS, a neurodegenerative disorder, at an alarming rate. The Department of Veterans Affairs confirms the findings using a different method, raising questions about environmental exposures during the war and potential links to Gulf War syndrome.
Researchers at Johns Hopkins and Salk Institute develop gene therapy that slows progression of amyotrophic lateral sclerosis (ALS), a devastating disease affecting thousands. In experiments with mice, injection of insulin-like growth factor-1 (IGF-1) into muscles extends survival and improves strength.
Researchers at Project A.L.S. have successfully tested a gene therapy approach that delays disease progression and prolongs survival in a mouse model of ALS. The treatment uses an adeno-associated viral vector to express the IGF1 protein, promoting neuronal survival.
Researchers found that injecting a gene producing insulin-like growth factor-1 (IGF-1) into muscles delayed disease onset by 31 days, preserved nerve cells, and reduced muscle wasting. This study may lead to a new, gene-based treatment for ALS affecting over 30,000 Americans.
A new three-year grant will help researchers better understand the causes and risk factors of ALS, a neurodegenerative disease that affects 30,000 people in the US. The study aims to investigate the link between a genetic mutation called Hfe and the onset and progression of ALS.
Researchers used 3D imaging to study ALS mutant proteins, finding they interact incorrectly and form toxic complexes that interfere with nerve cell function. The study supports two theories: oxidative damage from mutant SOD1 protein and aggregation of protein complexes.
Researchers have discovered a genetic link between specific mutations in the Dnchc1 gene and selective death of motor neurons, causing diseases like ALS. The study provides new insight into the pathogenetic mechanism underlying MND.
Researchers identified chromosomal abnormalities in 5.9% of ALS patients, suggesting a previously unknown risk factor for the disease. The study highlights the need for systematic genetic analysis of patients with ALS and other neurodegenerative diseases.
Researchers discovered a gene, Hsp27, that protects mature nerve cells from death following injury. Delivering this gene via therapy may lead to new treatments for neurodegenerative diseases and nerve injuries.
Researchers have found that growth factors play a key role in regulating how embryonic nerve cells acquire the ability to process information. This study suggests possible avenues for treating damaged nerve cells and restoring their function.
Scientists have found a gene responsible for a rare form of hereditary spastic paraplegia, a condition that slowly robs children of their ability to walk. The discovery has opened the door to better diagnosis and treatment of the disorder, as well as insights into other spinal cord problems.
A second gene mutation for the inherited form of ALS has been discovered by Northwestern University researcher Teepu Siddique. The newly identified gene, alsin, is responsible for juvenile inherited ALS (ALS2), a rare and slowly progressive disease affecting young populations in North Africa and the Middle East.