Articles tagged with Neurodegenerative Diseases
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A team of Canadian researchers has discovered the crucial function of a protein in Batten's disease, a neurodegenerative genetic disorder that affects children. The study found that the protein plays a vital role in maintaining cellular endosomal function, which can lead to degeneration if disrupted.
Researchers found that a specific type of immune cell accumulates in older brains and that activating these cells improves the memory of aged mice. Activating these cells also increases the formation of new nerve cells in the hippocampus and reduces inflammation.
Researchers developed a novel gene-silencing approach to deliver a treatment vector to adult ALS mice, preventing disease onset and blocking progression in animals with existing symptoms. The method uses an adeno-associated virus to deliver shRNA, effectively silencing the SOD1 gene and protecting motor neurons.
A new study reveals that spinocerebellar ataxia type 7 (SCA7) originates from metabolic dysregulation leading to altered calcium homeostasis in neurons. The research also identifies Sirtuin 1 as a key player in promoting calcium regulation and reducing neurodegeneration.
A Belgian-American research team has uncovered a new mechanism of neurodegeneration in Charcot-Marie-Tooth disease, revealing that tRNA synthetases can interfere with gene transcription in the nucleus. This discovery could lead to new therapeutic approaches for CMT patients.
Researchers discovered a phenomenon in brain cells where mitochondria 'eat themselves up' at an early stage of neurodegeneration. The study found that this self-destruction is selectively present in neurons prone to degeneration in ALS patients, providing potential targets for new therapies.
Researchers at Northwestern University have discovered a new phenomenon in the brain where mitochondria self-destruct, leading to early stages of neurodegeneration. The study found that this process occurs selectively in neurons vulnerable to future degeneration, providing a potential target for drug therapies.
Researchers suggest 'Havana Syndrome' is akin to shell shock, with symptoms paralleling those of war trauma. Studies on embassy patients found no conclusive evidence for exposure to an energy source or toxin.
Researchers at Barrow Neurological Center discovered aberrant RNA processing in ALS and FTD patients, led by Dr. Rita Sattler's team finding ADAR2 mislocalization affects disease pathways, potentially leading to neuronal loss and neurodegeneration.
The study analyzed 26 widely-used protein disorder prediction methods and found that they vary noticeably in performance. This thorough comparison provides valuable insights for protein scientists to make informed choices about which programs to use.
The ALS Association has committed an additional $3.5 million to the NYGC's CGND, while The Tow Foundation has contributed $2.5 million, renewing support for genomic research and patient data analysis. These investments aim to accelerate the development of new treatments and a cure for ALS.
A team of scientists has successfully cloned gene-edited monkeys with disease phenotypes using somatic cell nuclear transfer. The monkeys, which exhibit circadian disorder phenotypes, can be used to study the pathogenesis and therapeutic treatments for human diseases such as sleep disorders and neurodegenerative diseases.
Research has confirmed the presence of neurotoxin BMAA in 89% of eastern Australian freshwater samples, with highest levels ever recorded. The toxin is produced by cyanobacteria and linked to neurodegenerative diseases such as ALS/MND worldwide.
Researchers at University of Illinois Chicago used graphene to identify cerebrospinal fluid from patients with ALS, multiple sclerosis, or no neurodegenerative disease. The study found unique changes in graphene's vibrational characteristics depending on the patient's condition.
Researchers at St. Jude Children's Research Hospital have developed a new class of compounds called pantazines that may treat the rare neurodegenerative disorder pantothenate kinase-associated neurodegeneration (PKAN). The compounds elevate coenzyme A levels, preventing neuron dysfunction and improving symptoms in mice models.
A new PET imaging radiotracer, <sup> 18 </sup> F-XTRA, was tested on adults to study the distribution of the α4β2 nicotinic acetylcholine receptor in the brain. The research found that the radiotracer rapidly entered the brain and distributed quickly, with lower binding in the hippocampus with healthy aging.
A protein called Staufen1 accumulates in cells of patients with degenerative ataxia or amyotrophic lateral sclerosis (ALS), suggesting a potential therapeutic target. Depleting Staufen1 from affected mice improved symptoms, revealing a novel avenue for treating neurodegenerative diseases.
Researchers discovered the intrinsically disordered region (IDR) of Ataxin-2 facilitates its association with other pathogenic proteins, contributing to ALS and SCA2 progression. It also plays a vital role in long-term memory formation and rewiring the nervous system.
Microglia, specialized immune cells in the brain, have been found to gobble up the remnants of injured neurons, preventing damage from spreading to neighboring neurons. This discovery could lead to new strategies for boosting microglial clearance and limiting neurodegeneration after brain or spinal cord injury.
A study from McGill University found that combining probiotics with an herbal supplement called Triphala increases fruit fly lifespan by 60%. The researchers observed reduced traits of aging, including insulin resistance, inflammation, and oxidative stress. The findings suggest a potential link between gut bacteria and human longevity.
The xB3 platform efficiently delivers antibodies across the BBB, maintaining systemic pharmacokinetics and improving brain exposure. The platform demonstrates dose-dependent effects in neuropathic pain models, providing a promising treatment for CNS disorders.
Scientists have developed a new drug compound that shows promise as a future treatment for Charcot-Marie-Tooth disease, an inherited neurodegenerative condition affecting peripheral nerves. The researchers found that the problem lies in mitochondria's inability to travel distances, leading to nerve atrophy and muscle loss.
A study led by Patrick Freund found that patients with smaller initial nerve loss have better long-term recovery. The researchers tracked microstructural changes in the spinal cord and brain after two years, predicting recovery trajectories using non-invasive neuroimaging.
A new study provides the first 3D visualization of the dynein-dynactin complex bound to microtubules, revealing a surprising feature: two dynein molecules where one was expected, with four motor domains total. This discovery helps explain how dynein can haul large loads over long distances in crowded cellular environments.
Researchers have developed a novel laboratory model that replicates key hallmarks of pediatric high-grade glioma, a devastating illness and leading cause of death in children. Mutations in histone 3.3 are believed to play a pivotal role in its development, with the new model supporting the concept that cancer starts in utero.
A team of Japanese and US scientists have created a microdevice that successfully forms axon fascicles in the lab, similar to those seen in the brain. This innovation could provide insights into brain development and disease prevention by studying the formation of fascicles.
The study seeks to discover calcium sources in synapses that prolong neurotransmitter release, a process more expressed in neurodegenerative diseases. Researchers will investigate key players in this process using asynchronous release of neurotransmitters.
Researchers have discovered a new role for an enzyme called Axundead in promoting axon degeneration. However, blocking its function preserved the integrity of injured axons and allowed them to maintain signal transmission within the brain's complex circuitry for weeks.
A study by Sanford Burnham Prebys Medical Discovery Institute researchers found that autophagy declines with age, leading to incomplete recycling of cellular waste. The team discovered this decline occurs after autophagosomes are formed, potentially blocking the conversion process and contributing to age-related diseases.
Researchers discovered two brain proteins with unique functions in the development of dementia, leading to potential new treatments. The study used Drosophila fruit flies to examine the effects of these proteins on nerve cell survival and activation, revealing one form is linked to poor movement and another to greater neurodegeneration.
Dendritic cells are crucial for immunity against pathogens and foreign substances. Researchers found that these cells develop from specialized progenitors, not a common progenitor, providing insights into the regulation of human immune responses.
A new study reveals that circular RNAs, previously thought to be non-coding, can encode for proteins. The discovery suggests an unexplored layer of gene activity and may have implications for understanding aging and neurodegenerative diseases.
Researchers at Toronto Western Hospital's Canadian Concussion Centre discovered CTE in a brain without head trauma or concussion history. The finding suggests that the cause of CTE might be more complex than previously thought, with Dr. Lili-Naz Hazrati stating that there are more questions than answers about the definitive causes of CTE.
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 Scripps Florida team has been awarded $1.8 million to develop drug candidates for diseases such as heart disease, rheumatoid arthritis, and neurodegenerative disorders. The researchers will focus on inhibiting the ASK1 enzyme, which has shown promise in reducing heart cell death and improving resistance to stress-related diseases.
Researchers discovered a link between genes nardilysin and OGDHL, which are crucial for mitochondrial function, and progressive loss of neurological functions in humans. Mutations in these genes lead to neurodegeneration, characterized by the accumulation of cellular trash.
Researchers at Tel Aviv University found that phosphatidylserine treatment can enhance the stability of microtubular highways in neurons and improve cargo movement along these pathways. The study suggests that this supplement may be instrumental in reversing detrimental effects of Familial Dysautonomia.
Researchers at the University of Minnesota have made a groundbreaking breakthrough in developing a noninvasive brain-computer interface technology that allows people to control a robotic arm using only their minds. Eight healthy human subjects successfully controlled a robotic arm to pick up objects and move them from one location to a...
The grant will accelerate the creation of high-priority mouse models for Charcot-Marie-Tooth disease and other peripheral neuropathies. Researchers aim to investigate disease mechanisms and develop treatments, which currently have no cures or effective treatments.
Researchers at Tokyo Institute of Technology have discovered the molecular mechanism behind autophagy initiation, revealing that Atg13 forms a supramolecular complex with other proteins. This breakthrough may lead to the development of therapeutic treatments for diseases such as neurodegeneration and cancer.
Research suggests that patients with MSA have lower levels of coenzyme Q10 (CoQ10) in their blood, regardless of COQ2 genotype. This finding may support the idea that CoQ10 supplementation could be beneficial for MSA patients. However, more studies are needed to confirm this hypothesis.
Scientists create method to differentiate patient-derived stem cells into retinal ganglion cells, which can help combat neurodegeneration in glaucoma. This breakthrough enables personalized medicine prospects for patients with glaucoma.
Researchers have elucidated the structure of mTORC1, a crucial protein complex involved in cellular signaling and disease regulation. The study reveals detailed interactions between partner proteins, shedding light on the mechanism of rapamycin-induced changes, which affects substrate specificity and pharmaceutical effects.
Researchers at Mayo Clinic found significant evidence of chronic traumatic encephalopathy (CTE) in males who participated in amateur contact sports, including football, wrestling, and rugby. The study suggests that these sports may increase the risk of developing CTE, a progressive degenerative disease caused by repetitive brain trauma.
A fruit fly model of Alexander disease has been developed to study astrocyte dysfunction and its role in neurodegeneration. Nitric oxide has been identified as a critical mediator in the process.
A mutation in a key enzyme affects sphingolipid levels, leading to neurodegeneration. Researchers found that increased 20-carbon sphingolipids cause problems with neuronal membranes.
Research suggests that ALS patients consume more daily calories but have a lower body-mass index (BMI) than those without the disease. Higher premorbid intake of total fat, saturated fat, trans-fatty acids, and cholesterol is associated with an increased risk of ALS, while higher alcohol intake is linked to a decreased risk.
Researchers at NIH's NINDS have discovered a critical transport defect in motor neurons with SOD1 mutations, which causes cells to accumulate damaged materials. Increasing snapin levels during early stages of the disease can correct the problem and improve motor neuron survival.
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.
Scientists confirm neuroprotective function of PrPC against epilepsy using four animal models, revealing its crucial role in preventing seizures. The study's precision and collaboration between international institutes make it a significant reference point in the field.
A new study reveals how synchronized gene activation is achieved in developing neurons through a TTP/miR-9 regulatory pair, which limits messenger destabilization and ensures coordinated accumulation of neuronal proteins.
Researchers identified a cellular mechanism that can be targeted to treat ALS by increasing levels of protein hUPF1, which successfully protected against cell death in both genetic and sporadic versions of the disease. Treating this pathway may also have implications for frontotemporal dementia.
Researchers discovered a feedback signalling mechanism responsible for changes in nerve cells exposed to prolonged light, which may help protect neurons from degeneration. The study provides insight into synaptic plasticity and potential therapeutic applications for neurodegenerative diseases.
A breakthrough study discovered a novel neurodegenerative disease in Lagotto Romagnolo dogs caused by an ATG4D gene mutation. The research sheds light on the function of neurons and may aid in developing treatments for neurodegenerative disorders, as similar mutations have been linked to human diseases.
Researchers identify molecular pathway reducing misfolded proteins implicated in ALS and dementia. Inactivating specific genes can improve mobility in roundworms and human cells, suggesting potential therapeutic value.
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.
Researchers aim to target autophagy pathway, a key enzyme involved in cancer and neurodegenerative diseases. They plan to use high-throughput screening facilities to identify new inhibitors of Ulk1, a critical on-off switch regulating the pathway.
Researchers found lipid droplet accumulation in glial cells before signs of neurodegeneration appeared, leading to impaired support for neurons. Reducing components of the pathway can delay neurodegeneration.
A study of 219 MS patients found that only 46% maintained no-evidence-of-disease-activity for clinical and MRI measures at one year, decreasing to 27.5% at two years and 7.9% after seven years.
Researchers have made a breakthrough in understanding brain cell communication and developed a fruit fly model to study neurodegeneration. By partially inhibiting the breakdown of 'defective' proteins, they were able to completely suppress neurodegeneration in fruit flies.