Researchers have shed light on the relationship between misfolded alpha-synuclein protein and Parkinson's disease, identifying key genes and cellular processes involved. The study provides new insights into the underlying mechanisms of synucleinopathies, paving the way for developing patient-specific treatments.
A Norwegian study from the University of Bergen has identified key mechanisms behind Parkinson's disease, which may lead to future treatments. The research suggests that mitochondrial DNA damage is a primary cause of the disease, and that healthy brain cells can compensate for this damage by producing more DNA.
A synthesized steroid called squalamine has been shown to prevent the buildup of a lethal protein implicated in neurodegenerative diseases like Parkinson's. In an animal model, squalamine reduced the toxicity of alpha-synuclein clumps and protected healthy human neuronal cells from damage.
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Researchers found that squalamine inhibits the early formation of toxic alpha-synuclein aggregates and suppresses their toxicity. The compound was tested in cell cultures, animal models, and human neuronal cells, showing promising results.
Researchers found that increasing niacin levels boosts NAD compound for energy generation and DNA repair, potentially protecting against Parkinson's. The study suggests repurposing cancer drugs to protect faulty mitochondria in Parkinson's disease.
Researchers found that chemicals extracted from prickly pear and brown seaweed improve cellular and animal models of neurodegenerative proteinopathies. The study suggests these substances may target pathways affected by multiple neurodegenerative conditions.
A laboratory study found that alpha-synuclein, a protein involved in Parkinson's disease, can travel from the brain to the stomach via specific nerve pathways. The protein was detected in gastric nerve terminals six months after its initial midbrain expression.
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A study of over 6.5 million Ontario residents found that those living within 50 meters of high-traffic roads had a seven percent higher likelihood of developing dementia compared to those further away. The risk increased with proximity, but not for Parkinson's disease or multiple sclerosis.
Duke University researchers have developed a new approach to deep brain stimulation that reduces energy consumption by up to 75% without compromising treatment efficacy. The algorithm uses computational evolution to design tailored patterns for individual patients, leading to improved symptoms and reduced battery replacement procedures.
Richard Myers is investigating the Cyclin G-associated kinase (GAK) gene and its role in Parkinson's disease. His research aims to understand how increasing GAK levels may prevent cell death in PD.
A study published in Neurology found that welders who work with manganese fumes are more likely to develop Parkinson's-like symptoms. The researchers analyzed data from 886 workers and found that cumulative exposure to manganese was associated with a yearly increase in movement problems.
Welders exposed to low levels of manganese exhibit neurological symptoms similar to Parkinson's disease, including slow movement and difficulty speaking. Current OSHA safety standards may not protect workers from the dangers of welding fumes.
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Researchers have found that activating the protein Nrf2 can restore normal levels of disease-causing proteins in cells, preventing cell death. In models of Parkinson's and Huntington's diseases, Nrf2 was shown to protect cells against the disease better than any other treatment.
Researchers at the University of Helsinki have successfully corrected Parkinson's disease motor symptoms in mice using a PREP blocker treatment. The treatment, which blocks the formation of alpha-synuclein aggregates, restored motor skills and cleared brain accumulations within two weeks.
A new study reveals that brain stimulation can improve timing abilities in mice lacking dopamine, a key player in Parkinson's disease. The breakthrough finding suggests that targeted brain stimulation could be used to treat cognitive problems caused by PD and possibly other conditions.
Researchers found significant alterations in brain networks of PD patients with mild cognitive impairment, indicating complex structural brain network disruption rather than individual white matter degeneration. The study suggests using MRI to monitor the disease and predict cognitive complications.
Researchers have developed a diabetes drug that slows experimental Parkinson's disease progression by regulating mitochondrial function and reducing inflammation. Human trials are set to begin next year, offering hope for the first treatment to target the underlying disease.
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Researchers detect misfolded alpha-synuclein aggregates in cerebrospinal fluid to diagnose Parkinson's disease. The Protein Misfolding Cyclic Amplification technology detects small amounts of the protein, correlating with disease severity.
Researchers at Caltech discovered a functional link between bacteria in the intestines and Parkinson's disease, showing that changes in gut bacterial populations contribute to motor skill deterioration. The study found that an imbalance in short-chain fatty acids regulates brain inflammation and symptoms of PD.
A study found that gut microbes exacerbate motor symptoms in a mouse model of Parkinson's disease, but antibiotic treatment and germ-free environments reduced motor deficits. The research could lead to new treatments for the neurodegenerative disease.
Researchers at Caltech discovered a novel link between the gut microbiome and Parkinson's disease, finding that gut bacteria promote hallmark pathology, neuroinflammation, and motor dysfunction. The study suggests targeting the gut microbiome may provide a new approach for diagnosing and treating PD.
A new study finds that GBA gene mutations are associated with increased cognitive decline in Parkinson's patients, who carry one defective copy of the gene. Patients with a more severe mutation showed a 217% increased risk of cognitive impairment within ten years of diagnosis.
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Researchers have made a breakthrough discovery on the formation and dissociation of pathogenic α-synuclein fibrils in Parkinson's disease, providing new insights into its progression. The study shows how high hydrostatic pressure breaks apart these toxic fibrils, shedding light on potential strategies for treating PD.
Patients with Parkinson's disease exhibit significant cognitive deficits when experiencing a drop in blood pressure upon standing up, known as orthostatic hypotension. These deficits reverse when they lie down and their blood pressure returns to normal.
Researchers at Iowa State University found a gene mutation linked to an accelerated onset of Parkinson's disease in Caucasians, with those under 50 experiencing symptoms 5 years earlier and a 45% increased risk. The study also highlights the importance of blood cholesterol levels, which are directly related to dopamine production.
Researchers used whole-brain MRI mapping to reveal pathological alterations in brain iron distribution. They found excess iron in areas like the substantia nigra and decreased iron content in previously overlooked regions, such as the dentate nucleus.
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Researchers developed a new imaging technique that allows studying protein misfolding and toxicity in neurodegenerative diseases. The technique enables visualizing changes in protein molecules' surfaces, shedding light on the mechanisms behind these devastating diseases.
Researchers explore therapeutic interventions like light, sound, and electrical energy to resynchronize damaged neurons in the brain. Neuroplasticity can be harnessed to treat a range of conditions, from bad habits to chronic pain syndromes.
A collaboration of 32 researchers found a genetic mutation in the PINK1 gene that confers a risk for developing Parkinson's disease earlier than expected. The study showed that a specific mutation impairs the PINK1-PARKIN pathway, leading to damaged mitochondria accumulation and neurodegeneration.
Researchers found that combining virtual reality with treadmill training reduced fall frequency and risk for at least six months after training. The intervention improved both physical mobility and cognitive aspects of safe walking.
Researchers discover a cellular mechanism by which brain deactivates and then gradually reactivates neurons in the temporal association cortex. This discovery challenges the idea that all neurons are present and fully active from birth.
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Researchers have adapted a facial analysis software to quantify how often patients' eyes closed when instructed to keep them open, finding a correlation with clinician ratings. The new program has the potential to help study facial tics and twitches in other contexts, including Tourette Syndrome, schizophrenia, and Parkinson's disease.
A recent study suggests that an enzyme deficiency in Krabbe's disease could contribute to mechanisms underlying Parkinson's disease and other neurodegenerative disorders. The protective myelin coating around nerve cells is compromised due to galactosylceramidase deficiency, a condition with currently no cure.
Researchers at the University of Copenhagen have found that adding the substance NAD+ to mice and roundworms can extend life and delay aging processes. The study suggests that NAD+ plays a key role in maintaining cellular health and repairing genes, with potential benefits for patients with Alzheimer's and Parkinson's disease.
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A team of scientists identified how amyloid beta, associated with Alzheimer's, can induce cellular changes leading to Parkinson's. This discovery may provide an explanation for the co-occurrence of these neurodegenerative conditions and help researchers find ways to prevent such cases.
CVT-301, an inhaled form of levodopa, is being studied for its potential to restore motor function in people with Parkinson's disease experiencing OFF periods. The Phase 3 clinical program aims to confirm the efficacy and safety profile of CVT-301.
Researchers at Johns Hopkins Medicine identified a protein that enables toxic alpha-synuclein aggregates to spread in the brain. A treatment strategy blocking this protein's action may slow Parkinson's disease progression, as antibodies already in clinical trials for cancer therapy show protective effects.
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Researchers found that exposure to bacterial proteins can cause brain proteins to misfold and lead to inflammation in the brain. The study suggests that gut bacteria may play a role in initiating these diseases, potentially leading to new treatments.
A massive MRI study identified seven genetic hotspots regulating brain growth, memory, and reasoning, as well as predicting the onset of Parkinson's disease. The research supports the notion that brain size can be used to measure 'brain reserve' and promote resilience to age-related brain diseases.
Researchers discovered that intestinal cells' immune response acts like detectives to identify damaged machinery within neurons and discard defective parts, protecting vital neurons. This innate mechanism, originating in the intestine, may hold the key to preventing Parkinson's disease.
A team of Stanford University School of Medicine researchers discovered a critical defect that precedes the death of nerve cells in Parkinson's disease, impairing mitochondria function. This finding may lead to earlier diagnoses and new treatment approaches for the condition.
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Researchers have found that specific mutations in Parkinson's disease protein alpha-synuclein can dramatically affect microscopic processes leading to the condition's onset. The study suggests these tiny changes influence fibril formation and secondary nucleation, potentially contributing to the disease's development.
Researchers at the University of Edinburgh have developed a way to detect alpha-synuclein, a protein linked to Parkinson's disease, in spinal fluid samples. The new test shows promise in identifying patients with Parkinson's and Lewy body dementia in early stages.
α-synuclein aggregates are transported between neurons via lysosomal vesicles in tunneling nanotubes, enabling Parkinson's disease progression. This discovery highlights the role of tunneling nanotubes in intercellular communication and lysosome-mediated protein disposal.
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A study published in Neurology tracks neural changes in patients with Parkinson's disease and two similar conditions over time. Researchers found decreased activity in specific brain regions, which could provide a new tool for testing experimental medications.
Researchers developed a non-invasive way to track Parkinson's disease progression using functional magnetic resonance imaging, revealing areas of progressive brain decline. This biomarker could help evaluate experimental treatments and measure neurological changes behind symptoms.
Combining virtual reality and treadmill training reduces fall rates in older adults, with a 42% decrease in the virtual reality plus treadmill group compared to treadmill training alone. This intervention has potential as part of prevention packages for falls risk before injuries occur.
A new laboratory model of Parkinson's disease has successfully replicated the phase that occurs long before diagnosis, revealing how abnormal alpha-synuclein proteins spread in the brain. The study demonstrates a possible link between Parkinson's and non-motor symptoms like cognitive impairment and gastrointestinal issues.
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Researchers recorded neural activity in human striatum, a key structure compromised in Parkinson's disease. The study provides new understanding of pathophysiology and potential treatments for PD.
A new review explores potential antioxidant approaches for Alzheimer's, Parkinson's, and other neurodegenerative diseases. Certain compounds targeting oxidative stress pathways, such as Nrf2, are being investigated.
Scientists have developed a new method to measure the activity of disease-causing mutations in the LRRK2 gene, a major cause of inherited Parkinson's disease. The breakthrough could help pave the way for a clinical test that could facilitate evaluation of drugs targeting this form of the condition.
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UAB researchers have discovered that levodopa induces widespread DNA methylation changes in brain cells that contribute to the development and maintenance of levodopa-induced dyskinesia. Modulating global DNA methylation may be a novel therapeutic target to prevent or reverse this condition.
A study published in Scientific Reports found tiny DNA changes linked to Parkinson's disease in unexpected places, including liver, fat, immune, and developmental cells. These findings suggest a diverse set of underlying causes for the disease, challenging current understanding of neurodegenerative disorders.
The Scripps Research Institute has received a grant to support safety and quality tests of a potential stem cell therapy for Parkinson's disease. The two-year project will investigate induced pluripotent stem cells derived from adult subjects, which can differentiate into dopamine-producing neurons.
Researchers have found an interaction between a mutant gene and alpha synuclein in neurons that contributes to Parkinson's disease pathologies. Drugs now under development may block the process by targeting LRRK2 kinase activity.
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Researchers developed a method to measure how the brain responds to electrical stimulation, allowing for more effective deep brain stimulation treatment. This patient-specific approach uses phase response curves to predict and optimize stimulus patterns, potentially improving efficacy and reducing side effects.
A review article argues that telehealth will transform healthcare delivery, providing access to care at a lower cost. The authors identify three trends reshaping telehealth: making care more accessible, expanding its application beyond acute conditions, and migrating from hospitals to home and mobile devices.
Researchers have identified a molecule, NCGC607, that shows promise as a possible treatment for Gaucher disease and Parkinson's disease. The molecule helps to break down cellular waste and reduce alpha-synuclein levels, suggesting a potential treatment strategy.
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Researchers found that an FDA-approved cancer drug increased brain dopamine and reduced toxic proteins linked to Parkinson's disease progression. The study showed significant signs of benefit for patients with neurodegenerative diseases, including improved cognitive and motor functions.
Researchers linked traumatic brain injury with later development of Parkinson's disease, but not Alzheimer's disease or incident dementia. The study, involving over 7,000 participants, found an association between TBI and Parkinson's disease, contradicting common assumptions about the relationship between TBI and Alzheimer's.