Articles tagged with Parkinsons Disease
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A single gene mutation in the LRRK2 gene has been identified as a cause of around one in 25 cases of Parkinson's disease worldwide. The mutation is associated with both inherited and sporadic forms of the disease, suggesting new diagnostic and treatment options on the horizon.
A new genetic mutation on the LRRK2 gene is responsible for 5% of inherited Parkinson's disease cases, with patients having longer disease duration but less severe symptoms. The discovery has a broad implication for genetic screening for the disease, highlighting the need to include studies of the LRRK2 gene in future testing.
A study found that a mutation in the LRRK2 gene appears in at least one of every 60 people with Parkinson's disease. The mutation may account for 1½ to 2 percent of cases, particularly those without a family history, and could lead to earlier detection of the disease.
A recent study found that the LRRK2 mutation is the most common genetic cause of Parkinson's disease, affecting approximately 5% of patients. This mutation is linked to slower disease progression, while symptoms are less severe compared to other mutations in the gene.
Researchers can submit study information to a new patient website, www.PDtrials.org, designed to improve access to Parkinson's clinical trial information. The site currently lists over 30 studies recruiting patients in the US and aims to educate patient communities on the value of clinical research.
Researchers successfully transplanted monkey embryonic stem cells to reverse Parkinson's disease symptoms in primates. The study demonstrated the potential of this approach to treat neurodegenerative diseases, despite low survival rates of transplanted neurons.
Researchers identified a novel oncogene in Chernobyl residents with papillary thyroid cancer, resulting from the fusion of the AKAP9 and BRAF genes. This study provides evidence that chromosomal inversions are a common molecular lesion in post-Chernobyl thyroid cancers.
A recent study published in NEJM found that levodopa did not accelerate Parkinson's disease progression but may actually slow it. The multi-center trial involved 361 newly diagnosed patients and showed a clear-cut benefit of levodopa, with higher dosages producing more beneficial results.
Researchers found that brain surface stimulation significantly reduced Parkinson's symptoms in animals, restoring normal activity in the striatum and motor cortex. The study suggests that this method could be an effective alternative to deep-brain stimulation with major advantages in simplicity and safety.
Researchers found that viral delivery of a parkin gene protected dopamine-producing neurons from degeneration, offering new hope for treating Parkinson's disease. The study demonstrates the feasibility of gene therapy in a genetic model of the disease.
Researchers found that rifampicin stabilizes alpha-synuclein in a soluble form, preventing fibril formation and disaggregating existing fibrils. This finding suggests potential therapeutic benefits for Parkinson's disease when administered early in the disease process.
Researchers found a mutation in the LRRK2 gene that plays a central role in developing Parkinson's disease and other neurodegenerative disorders. The discovery has major implications for understanding mechanisms of these diseases and potentially leading to curative treatments.
Chronic exposure to pesticides like rotenone has been linked to Parkinson's disease pathology in monkeys. Exercise has shown potential in protecting against dopamine neuron loss and slowing disease progression in rats. Rotigotine, a new drug, may also offer neuroprotective properties.
A study in rats found that exercising limbs can protect brain cells from degeneration caused by Parkinson's disease. Exercise was shown to increase the production of key proteins that promote neuronal survival, such as glial cell line-derived neurotropic factor (GDNF), which may help offset cell vulnerability to oxidative stress.
Researchers pinpointed a specific gene, dardarin, causing PARK8-linked Parkinson's disease, affecting approximately 8% of Basque people with PD. The mutation is expressed throughout the brain and has characteristics of a molecular switch, suggesting a potential role in protein phosphorylation.
Scientists have identified two genetic mutations in the PARK8 gene that contribute to Parkinson's disease, a condition characterized by tremors and motor impairments. The discovery provides new insights into the molecular mechanisms underlying the disease and may lead to targeted interventions.
Researchers found that bilateral motor performance improvements were seen in patients with Parkinson's disease, regardless of where the stimulation was applied. The study suggests that unilateral deep brain stimulation could be a more effective and lower-risk treatment option for some patients.
A study by Johannes Schwarz and colleagues tracked molecular changes in brains of Parkinson's patients over 7.5 years using SPECT to measure dopamine transporter binding, revealing a single exponential decline rather than linear loss. This advancement enables the development of individualized treatment for advanced Parkinson's patients.
Research by FSU scientist Cathy Levenson reveals that dietary iron imbalances trigger a chain of cellular events increasing the risk of developing Parkinson's disease. Excessive iron levels precipitate symptoms in healthy mice, while low levels delay onset and slow disease progression in those already infected.
The grant will fund research on dopamine neurons and brain adaptation in Parkinson's disease, with the goal of developing new treatments for patients. Northwestern University's expertise in neuroscience and molecular imaging will be utilized in this effort.
Researchers created a mouse embryonic stem cell model to study Parkinson's disease, revealing that DJ-1-deficient cells exhibit heightened sensitivity to oxidative stress. The model also linked DJ-1 dysfunction to alpha-synuclein aggregation, a hallmark of Parkinson's neuropathology.
Parkinson's disease is often associated with depression, a condition that can significantly impact patients' lives. Research suggests that depression is part of the illness and not just a reaction to the disease.
Researchers at Cedars-Sinai Medical Center have found that Sonic Hedgehog and Gli-1 proteins delivered to lab rats via a genetically engineered virus prevented progressive nerve cell loss in the brain. This study may lead to a new way to treat patients with advanced Parkinson's Disease.
Researchers at Columbia University Irving Medical Center discovered that mutant alpha-synuclein protein causes blockage in dopamine neurons, leading to their death and eventually Parkinson's disease. This finding may aid in the development of new treatments to slow or stop disease progression.
The study found that pramipexole and levodopa both significantly reduced motor complications and improved functional outcomes. However, pramipexole had a lower risk of dyskinesias and wearing off compared to levodopa. Both treatments provided similar quality of life, but long-term follow-up is needed to determine superiority.
Researchers found a moderate association between the APOE-2 gene and an increased risk of developing Parkinson's disease, with a 20% higher chance. In contrast, the APOE-4 gene was not linked to Parkinson's disease, contrary to its established role in Alzheimer's risk.
A study of 97 Parkinson's disease patients found that those with elevated homocysteine levels were more depressed, had worse cognitive functioning, but no difference in physical functioning. High homocysteine levels are likely due to the use of levodopa in these patients.
Researchers have found that proteasome inhibitors can cause a model of Parkinson's disease in rats, mirroring symptoms such as slowness of movement and tremors. The study suggests that environmental factors, including exposure to toxins, may contribute to the development of Parkinson's.
Researchers developed a regulatable gene therapy that can be turned on and off using doxycycline, offering potential for treating Parkinson's disease. The treatment uses the glial cell line-derived neurotrophic factor (GDNF) protein to promote survival and differentiation of dopamine neurons.
A study found that 18% of early-onset Parkinson's disease patients have a single parkin gene mutation, raising questions about the clinical implications of this finding. The study's results challenge the long-held assumption that two mutations are required to develop Parkinson's disease.
A recent OHSU study found that Parkinson's caregivers experience dramatic declines in physical and mental health over 10 years, with increased strain and depression. The study identified predictors of caregiver risk, highlighting the importance of supporting family caregivers to improve patient outcomes.
A study by OHSU found that methylphenidate, Ritalin, increases the effects of levodopa on dopamine levels, improving symptoms such as tapping and walking speeds. In contrast, paroxetine had no effect on physical symptoms but increased walking speed in Parkinson's patients.
Researchers presented promising results of a long-term gene therapy trial in monkeys with Parkinson's disease, showing improved symptoms with reduced levodopa doses. Genetic studies identified a new risk factor for early symptom onset linked to the GST gene, emphasizing the importance of both environmental and genetic factors in PD dev...
Researchers have found that dental pulp cells can provide support and survival for nerve cells affected in Parkinson's disease, potentially leading to a new cell-based therapy. The study suggests that these cells produce beneficial 'neurotrophic' factors, promoting nerve cell survival.
A recent study by American Academy of Neurology found that patients taking pergolide for Parkinson's disease have a higher risk of developing valvular heart disease. Eighty-nine percent of pergolide-treated patients showed some degree of valvular insufficiency, with increased risks in the mitral and aortic valves.
A new study has found that the APOE-2 form of the gene increases the risk of developing Parkinson's disease by 20 percent compared to other forms of the gene. The study analyzed data from 22 studies and 9,988 participants, providing strong evidence for the link between the APOE gene and Parkinson's disease.
A new study found that infusing a molecule called glial cell line-derived neurotrophic factor (GDNF) directly into the brain improved Parkinson's disease symptoms in 41% of patients. The GDNF infusion resulted in significant increases in dopamine production and was sustained for at least two years, according to the research.
Researchers analyzed brains of deceased men with Parkinson's disease and found a significant decrease in neurons compared to those without the disease. The study suggests that neuron loss starts approximately 13 years before diagnosis, paving the way for potential preclinical intervention.
Researchers at Johns Hopkins Medicine discovered that nitric oxide attaches to parkin protein, reducing its ability to mark proteins for destruction. This process may contribute to Parkinson's disease progression, providing a potential new target for treatment.
Researchers have identified a novel gene linked to familial Parkinson's disease, revealing a new pathway for therapeutic treatment. The discovery places mitochondrial function at the centre of Parkinson's research, particularly in relation to oxidative stress and brain cell degeneration.
A 12-month quality of life study with Parkinson's patients shows significant improvement in movement and quality of life after receiving a transplant or sham surgery, regardless of actual treatment. The study suggests that the placebo effect plays a crucial role in this disease.
Researchers discovered a protective protein, Wlds, that safeguards dopamine-axon connections in Parkinson's disease. The study revealed that while the protein protects axons, it does not prevent cell body damage, highlighting differences in degeneration processes.
Researchers at UVA Health System have developed a cellular model of Parkinson's disease that can be used to study the disease's pathological features and test potential treatments. This model replicates the characteristic Lewy bodies found in brain tissue from patients with advanced Parkinson's disease.
Researchers aim to identify a gene on chromosome two linked to Parkinson's disease in families with multiple affected members. The study, called PROGENI, will enroll an additional 300 sibling pairs to investigate genetic risk factors for the neurodegenerative disease.
A clinical trial found that low-dose clozapine can reduce levodopa-induced dyskinesias (LIDs) in people with severe Parkinson's disease by around 50 percent. The study suggests that clozapine may mitigate the transmission of toxically high levels of levodopa, thereby reducing its potency and lessening the severity and duration of LIDs.
Researchers developed a system using a tri-axial accelerometer and fractal analysis to study Parkinson's patients' walking patterns. The study reveals the complexity of body motion in both healthy elderly subjects and Parkinson's disease patients, with the latter exhibiting higher fractal measures indicating more complex symptoms.
A yeast model study has identified a key link between alpha-synuclein protein overexpression and Parkinson's disease, shedding light on the protein's role in neurodegeneration. The research found that doubling the expression of alpha-synuclein gene in yeast cells led to toxic inclusion bodies causing cell death and neurodegeneration.
Researchers used baker's yeast to model Parkinson's disease, showing how a small amount of alpha-synuclein protein can cause deadly clusters. The study may lead to improved quality-control mechanisms in cells that normally dispose of misfolded proteins.
A recent Neurology journal study has identified levodopa addiction in non-parkinsonian patients, suggesting the potential for addiction to this common Parkinson's disease treatment. Additionally, researchers have discovered RNA gene slicing mutations in McArdle patients, revealing new insights into neuromuscular diseases.
Researchers found that patients with Parkinson's disease performed better when their stimulators were turned off in tasks requiring spatial memory and inhibitory control. The study suggests that adjusting stimulation levels may be possible to minimize cognitive impairment while maintaining motor benefits.
Several commonly used pesticides are toxic to mitochondria in laboratory experiments, causing cellular damage that may contribute to diseases such as Parkinson's. The study found pyridaben to be the most potent toxic compound, followed by rotenone and fenpyroximate.
Researchers discovered a major new finding on the genetics of Parkinson's disease, focusing on the activity of alpha synuclein. The study found that an abnormal triplication of genes on chromosome 4 leads to excessive protein buildup, causing Parkinson's symptoms.
A study found that nearly 50% of Parkinson's patients on levodopa therapy experience 'wearing off' within one to two years, causing symptoms to re-emerge before the next dose. This phenomenon is associated with motor and non-motor symptoms, as well as autonomic nervous system dysfunction.
Researchers identified a single gene, glutathione S-transferase omega-1 (GSTO1), as a key factor influencing the age of onset for both Alzheimer's and Parkinson's diseases. The study used genomic convergence to narrow down the genome region associated with age at onset, providing potential new targets for treatment.
Researchers have discovered that smaller protein structures called protofibrils are more toxic to cells than mature fibrils in type II diabetes and other age-related diseases. The study suggests that targeting earlier stages of protofibril formation may be a more effective approach to developing treatments.
Researchers found that relatives of people with tremor-dominant Parkinson's disease and those with postural instability gait disorder are more likely to experience action tremor. The study provides insight into the genetic influence of Parkinson's disease.
Researchers at Thomas Jefferson University and the University of Michigan have identified a gene defect behind a devastating muscle-wasting disease. The study found that a mutation in the Omi/HtrA2 protein causes neuronal cell death by impairing mitochondrial function.
A long-term follow-up study found that deep brain stimulation on the subthalamic nucleus improved motor scores by an average of 48% and reduced medication requirements. Younger patients with advanced Parkinson's Disease experienced sustained improvement in motor function for up to two years.
Researchers at Memorial Sloan Kettering Cancer Center have successfully differentiated stem cells into genetically matched dopamine neurons, mimicking normal brain cell development. The breakthrough could lead to new treatments for Parkinson's-like disease in humans.
The STEPS study evaluates the safety and efficacy of Spheramine, a cell therapy that produces levodopa to enhance dopamine production in the brain. The study aims to provide a new method for Parkinson's patients to achieve continuous control of motor function.