Articles tagged with Paraplegia
A recent study published in Journal of Experimental Medicine found that immune cells play a major role in the development of spastic paraplegia type 15. The research, led by Professor Elvira Mass and Dr. Marc Beyer, suggests that severe inflammation in the brain precedes neuronal damage and could be relevant to Alzheimer's disease.
A team of researchers found bacteria linked to the gut in the brains of mouse models implanted with microelectrodes, breaching the blood-brain barrier. The discovery highlights the need for permanent strategies to prevent bacterial invasion from implanted devices, which can contribute to inflammation and reduced device performance.
Researchers have defined what a premature aging disease is and developed tools to diagnose progeria patients, allowing them to identify new syndromes. The study also identified correlations between progeroid syndromes and other conditions, providing a significant step forward in understanding premature aging.
Researchers develop nanovector nanogels that selectively target glial cells involved in spinal cord injury inflammation, reducing damage and improving recovery. The treatment demonstrates potential for modulating glial cells in neurodegenerative diseases like Alzheimer's.
Researchers found that severe spinal cord injuries can disrupt communication between the nervous system and immune system, leading to systemic immune deficiency. Blood markers associated with this deficit can help gauge individual vulnerability to infection.
A recent study in Columbus reveals striking disparities in accessibility for wheelchair users traveling by public bus. Manual wheelchair users have access to only 1% of the city, while powered wheelchair users can reach about 25%. The main obstacle is infrastructure, particularly sidewalks, which are damaged or missing in many areas.
A new research model allows scientists to study hereditary spastic paraplegias (HSPs) and test potential therapeutics. HSPs cause increased muscle tone in infants and young children, leading to wheelchair-bound individuals who lose motor function.
Hereditary spastic paraplegia is a rare disease affecting approximately 77,000 Europeans, causing leg spasms and weakness. Researchers have discovered that the disease is linked to reduced calcium regulation, disrupting transport processes in brain cells.
Scientists at the University of Warwick have discovered a new process that activates the fastest molecular motor in neurons, paving the way for new treatments. The research focuses on KIF1C, a tiny protein-based molecular motor that converts chemical energy into mechanical energy to transport cargoes along microtubule tracks.
Two patients with paraplegia regained the ability to walk with minimal assistance through a fully non-invasive brain-machine interface, producing over 4,500 steps. The technology combines EEG-based brain control with functional electrical stimulation to produce a smoother gait pattern.
A study published in American Journal of Physical Medicine & Rehabilitation found that mobility and self-care abilities are the greatest impactors on quality of life for spinal cord injury patients. The research, which analyzed data from 195 patients with traumatic spinal cord injury, revealed differences in priorities between tetraple...
Trevor Dyson-Hudson, MD, of Kessler Foundation, is honored for his outstanding contributions to improving the lives of individuals with spinal cord injury. He has made significant contributions to user guidelines for wheelchair maintenance and training, helping people remain active and confident.
Researchers link abnormal TOR activity to oxidative stress and degeneration in both muscle cells and neurons. This discovery has broad implications for understanding diseases such as Alzheimer's, cancer, and HSP, and may lead to new therapeutic targets.
Researchers identify KIF5A as a new gene associated with ALS, implicating the role of cytoskeletal defects in axon communication. The discovery suggests the cytoskeleton as a potential target for new drug development and may lead to improved treatments for familial and sporadic ALS.
Scientists at McGill University have identified novel gene mutations that cause hereditary spastic paraplegia (HSP), a debilitating disease characterized by weakness or spasticity in the lower limbs. The discovery will aid in the development of treatments for HSP, with researchers predicting improved diagnosis and treatment options.
Researchers at Vanderbilt University Medical Center are conducting a proof of concept experiment using intraspinal microstimulation technology to restore complex body movements in paralyzed patients. The study aims to identify the optimal sweet spot for stimulation along the spinal cord, which has shown promise in animal studies.
Michihisa Umetani, a University of Houston professor, has won a $5,000 grant from the Neuron-Genetics Institute to further research into hereditary spastic paraplegia type 5A. The prize will help him and his team investigate the role of 27-hydroxycholesterol in human physiology and disease.
Researchers found large droplets of triglycerides within neurons of mice modeling the disease, leading to potential therapies and a new investigative strategy. The study points to triglyceride metabolism as a key factor in hereditary spastic paraplegia.
A study published in Science has identified a genetic mutation in almost 75% of cases, linking HSP to other common neurodegenerative disorders like Alzheimer's and ALS. The research found over 50 families with autosomal recessive HSP, providing insight into the biological processes underlying these diseases.
Researchers develop mouse models of hereditary spastic paraplegia and distal renal tubular acidosis to understand the molecular mechanisms underlying these diseases. The studies reveal key roles for REEP1 in ER shaping and β-intercalated cells in maintaining fluid and electrolyte balance.
Researchers develop mouse model of hereditary spastic paraplegia linked to changes in endoplasmic reticulum structure associated with REEP1 mutations, which impair ER function. The new model provides insight into how ER morphology affects axon loss in HSP.
Rice University biochemist James McNew is probing the key protein atlastin in the genetic disorder HSP. The study aims to build up a better understanding of how atlastin works and why its defects cause HSP.
A team of researchers has associated mutations in the reticulon 2 gene with hereditary spastic paraplegia type 12. They discovered that these mutations likely cause neurodegeneration by disrupting ER-shaping proteins, providing new insights into this complex disorder.
Scientists discovered a gene mutation causing hereditary spastic paraplegia, which may provide clues to axon degeneration in conditions like multiple sclerosis. The study highlights new disease mechanisms that could lead to genetic counselling and testing for affected families.
A study from Rice University and Italy's Eugenio Medea Scientific Institute has shed light on the biochemical workings of atlastin, a protein linked to HSP. The research suggests that atlastin plays a crucial role in maintaining the health of long nerve cells affected by HSP.
Researchers at the NIH have identified a key role for the protein Slc23a1 in controlling vitamin C levels in mice, which is essential for perinatal survival. Additionally, they discovered that treating multidrug-resistant leukemia cells with a specific drug can resensitize them to glucocorticoids and other cytotoxic agents by activatin...
Scientists discovered that neurons and plant root cells may use a similar mechanism to grow, shedding light on the genetics of hereditary spastic paraplegias. The study proposes that defects in the endoplasmic reticulum shape may cause HSP, with potential applications in Arabidopsis research.
Scientists have identified a gene in mice that plays a central role in the development of corticospinal neurons, which degenerate in patients with ALS. The discovery provides insight into how stem cells in the brain become specific types of neurons.
Endovascular repair, using stent grafts to fix blood vessel injuries, is shown to save more lives and decrease chance of paraplegia compared to open surgery. This minimally invasive technique reduces mortality rates by half and diminishes risk of paraplegia by 75 percent.
Scientists at Duke University Medical Center have identified a gene defect linked to hereditary spastic paraplegia, a rare nervous system disease with no cure. The discovery could lead to the development of drugs targeting the defective gene and provide insights into other neurodegenerative diseases.
Researchers have successfully treated hereditary spastic paraplegia by delivering a normal paraplegin protein to spinal motor neurons via gene therapy. This approach improved motor function in mice and holds promise for treating other forms of peripheral nerve damage caused by genetic mutations.
Researchers developed a strategy to deliver PDGF-BB to cardiomyocytes using self-assembling peptide nanofibers, protecting them from injury and reducing infarct size. This approach holds promise for tissue regeneration after cardiac injury.
A genetic model for hereditary spastic paraplegia (HSP) disease has been developed, showing that the spastin gene regulates microtubule stability to modulate synaptic structure and function. The study found that specific drugs can remedy defects in synaptic function caused by changes in neuronal spastin levels.
Studies investigate relationships between energy expenditure, lean muscle mass, and upper-body strength in persons with SCI. Researchers also explore potential treatments for bowel movement issues, respiratory problems, and pain management.
Researchers have found that nerve degeneration in spastic paraplegia is associated with abnormal mitochondria and impairment of axonal transport, highlighting a potential target for therapeutic interventions. The study suggests that preserving mitochondrial function may help prevent axonal loss in this devastating condition.
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.
Researchers have discovered four new genes in the most unstable part of chromosome 15 that contribute to Prader-Willi and Angelman syndromes and hereditary spastic paraplegia. These findings can expand genetic diagnosis of these diseases, including prenatal genetic counseling.
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.