Articles tagged with Amyloids
Researchers at Tokyo University of Agriculture and Technology have discovered a novel amyloid protein, lipopolysaccharide binding protein (LBP), that induces amyloidosis in rats. This finding is significant as it may provide insights into the development of human amyloidosis and serve as a disease model for studying this condition.
Research at MIT's Picower Institute has shown that stimulating a specific brain rhythm via light or sound can reduce amyloid buildup and improve memory in Alzheimer's model mice. The technique, called GENUS, also shows promise in reducing inflammation and improving blood vessel function.
Scientists observed how alpha-synuclein protein variants change over time, identifying initial stages of protein aggregates linked to early onset familial cases. They also found evidence of which protein species are important for amyloid filament growth and distinct structures depending on the mutation.
A new study by MIT neuroscientists pinpointed the earliest emergence of amyloid protein plaques in the human brain, finding they correlate strongly with disease progression. The research uses a mouse model to track plaque development and shows that these regions eventually spread throughout the brain.
Researchers have developed a way to track the formation of soluble amyloid beta peptide aggregates implicated in the onset of Alzheimer's disease. The ruthenium-based fluorescent complexes bind to these aggregates, allowing researchers to monitor their progress and movements over time.
Researchers have discovered two short peptides that significantly improved memory and reduced physical changes in the brain of mice with Alzheimer's disease. The treatment uses a process of computer modeling and artificial intelligence to develop an optimized oral version of the drug, which could lead to new treatments for Alzheimer's.
Researchers found that resistance to ghrelin hormone is linked to cognitive impairments and memory loss in Alzheimer's disease. Activating both ghrelin and dopamine receptors simultaneously may help restore brain function and reduce lesions.
Researchers at Osaka University used X-ray imaging to visualize Lewy bodies in post-mortem brains and found α-synuclein aggregates with cross-β structure. This discovery supports the idea that Parkinson's disease is a systemic amyloidosis, with implications for diagnosis and treatment.
Researchers discovered that the 'Australian' familial mutation in the APP TM domain leads to increased production of pathogenic amyloid-β peptides, resulting in neurodegenerative disorder. The study provides insight into a potential mechanism of Alzheimer's disease pathogenesis.
Researchers reveal precise three-dimensional structure of amyloid fibrils from PI3K SH3 domains, shedding light on protein folding and misfolding processes. The findings have significant implications for understanding the causes of neurodegenerative diseases.
Researchers have discovered a second molecular zipper in the beta amyloid protein that may contribute to the formation of brain fibrils in Alzheimer's disease. This kinked form is more harmful and can initiate a cascade of events leading to dementia.
A new small molecule drug, DYR219, targets the early instigator of Alzheimer's disease by inhibiting DYRK1 kinase. This approach delays amyloid plaque formation and improves cognitive performance in hybrid mice bred to develop AD-like symptoms.
Researchers used a far-infrared free-electron laser to break down amyloid fibril aggregates, disrupting their rigid sheet-like structure and causing free peptides to form. This technique has potential applications in medicine, biomaterial engineering, and regenerative medicine.
A new study found that FDG-PET scans are a better indicator of cognitive performance when compared to PET scans that detect amyloid protein. This suggests that FDG-PET is more precise in clinical studies and may be available for routine use at modest costs.
The University of Tokyo researchers modeled the amyloid beta sheets causing Alzheimer's disease and found that atoms too far apart can still influence each other through electron neighborhoods. This discovery may help predict the true structure and behavior of molecules based on their chemical sequence.
A study published in the Proceedings of the National Academy of Sciences finds that polyphosphate induces the formation of amyloid fibrils from beta-2 microglobulin proteins in dialysis patients. High levels of polyphosphate promote the formation of thicker, more stable amyloid fibrils under normal pH conditions.
A new study found that low social engagement in elderly men and women is associated with greater cognitive decline over three years, particularly among those with high levels of brain amyloid-β. Researchers say social engagement may be an important marker of resilience or vulnerability in older adults at risk of cognitive impairment.
A study has identified a key connection between two damaging proteins in Alzheimer's disease: amyloid beta and tau. Immune cells called microglia may be the missing link between these proteins, which can cause brain tissue damage.
Researchers at MIT used NMR spectroscopy to determine the structure of glucagon fibrils, finding a novel antiparallel beta sheet conformation and steric zippers that make the protein stable. This discovery may lead to shelf-stable versions of the hormone, which is used to control diabetes.
Researchers have identified the underlying mechanism behind reduced brain blood flow in Alzheimer's disease, which is caused by pericytes contracting around blood vessels. The study suggests that keeping pericytes relaxed could be a key to treating the disease, with new treatments potentially targeting this area.
Researchers found that smarter, more educated people have a 'cognitive reserve' that helps them perform better at baseline, but this doesn't affect their actual decline rate. Higher education levels are associated with lower rates of Alzheimer's disease in midlife, regardless of age or brain amyloid beta protein levels.
A new protein, CAPON, has been linked to the connection between amyloid-β plaques and tau pathology in Alzheimer's disease. Accumulation of CAPON increases AD-related pathology, while deficiency reduces symptoms. The study uses novel mouse models to explore this link.
Researchers found that viruses, like respiratory syncytial virus, form protein corona layers on their surface when interacting with host biological fluids. These layers enhance viral infectivity and facilitate the formation of amyloid plaques associated with neurodegenerative diseases like Alzheimer's.
The Collaborative Research Centre SFB/Transregio 102 at MLU is expanding its scope to investigate hybrid polymers, a combination of synthetic and protein-based materials. The researchers aim to gain a better understanding of these novel molecules and their potential applications in medicine and materials research.
Researchers found that long-term antibiotic treatment alleviates Alzheimer's disease symptoms in male mice by reducing inflammation and slowing amyloid plaque growth. However, the same treatment had no effect on female animals, with changes in the gut microbiome leading to increased proinflammatory factors.
A University of South Florida study reveals cofilin plays an essential role in worsening tau pathology, leading to brain cell death and neurodegenerative disorders like Alzheimer's. The research proposes inhibiting SSH1 as a potential target for treating Alzheimer's disease.
Researchers found a truncated variant of the p53 protein, Δ40p53, forming amyloid aggregates in endometrial cancer cells. This finding promises new perspectives for treating Type 2 endometrial cancer, the most aggressive form of the disease.
Cognitively normal adults with elevated levels of amyloid-β exhibited mixed attitudes toward physician-assisted death, reflecting complex emotions and values surrounding end-of-life care. The study highlights the need for nuanced discussions about dying wishes and advance care planning in this vulnerable population.
Researchers discover that disrupting the interaction between amyloid precursor protein and cholesterol leads to neurodegeneration, swelling of synapses, and fragmentation of axons. This finding suggests a new theory on Alzheimer's disease, where amyloid precursor protein may be an accomplice to cholesterol deficiency.
Researchers have developed synthetic peptides that target and inhibit small, toxic aggregates of amyloid beta, implicated as the toxic elements behind Alzheimer's disease. The peptides reduce amyloid beta-triggered toxicity in human neural cells and inhibit oligomers in laboratory animal models.
A study of 11,400 patients with dementia or mild cognitive impairment found that amyloid PET imaging was associated with changes in clinical management within 90 days. The use of this imaging technique was reported in 55% of MCI patients and 70% of those with dementia.
A nationwide study found that amyloid PET imaging significantly influenced clinical management of patients with mild cognitive impairment and dementia. The technique altered diagnoses and treatment plans in nearly two-thirds of cases, more than double predictions.
A team of researchers has demonstrated a novel approach for nanoscale imaging of amyloid structures using Thioflavin T, allowing for precise visualization of proteins associated with Alzheimer's disease. The technique enables the observation of amyloid fibrils assembling and disassembling in response to drugs.
A new study explores the connection between poor sleep and Alzheimer's disease, revealing that sleep helps clear excess amyloid beta and tau proteins from the brain. Disruption of slow-wave sleep can cause a significant increase in these protein levels, suggesting that sleep plays a crucial role in preventing Alzheimer's development.
Researchers found that a unique combination of light and sound improved cognitive and memory impairments similar to those seen in Alzheimer's patients. The treatment also greatly reduced amyloid plaques in the brains of mice, clearing large swaths of critical brain areas.
Researchers at Gladstone Institutes discover that a blood-clotting protein called fibrinogen destroys connections between neurons in the brain, resulting in cognitive decline. This finding offers an alternative explanation for memory loss and cognitive decline in Alzheimer's disease.
Researchers found that genetically engineered protein 3K3A-APC protects against Alzheimer's-like symptoms in mice by reducing amyloid-β toxin accumulation and inflammation. The study suggests 3K3A-APC as an alternative therapy for early stage Alzheimer's disease.
Researchers discovered that PRIMA-1 reverses mutant p53 aggregate accumulation, leading to the restoration of native protein function. The compound's potential as an anticancer drug is highlighted by its phase II clinical trials and positive results in breast and ovarian cancer cell lines.
A team of scientists has uncovered the amyloid precursor protein's modulating effect on neuronal signal transmission through binding to a specific receptor. This finding may lead to new treatments for Alzheimer's and other brain diseases.
Scientists have elucidated the formation mechanism of amyloid-β substances, causative agents of Alzheimer's disease. They found that Aβ peptides tend to aggregate at hydrophilic/hydrophobic interfaces, forming β-hairpin structures that facilitate intermolecular hydrogen bonding.
A UCL-led study confirms that some vials of discontinued hormone used in medical treatments contained seeds of a protein implicated in Alzheimer's disease. The research found that these seeds can seed amyloid pathology in mice and supports the team's hypothesis that amyloid beta was accidentally transmitted to patients via this treatment.
A new dye has been developed to detect signs of neurodegenerative diseases earlier and with greater precision. The dye can bind to specific amyloid structures in medical samples, allowing for the early detection of brain disease.
A recent study by the University of Helsinki reveals that pathological tau triggers a safety valve mechanism in cell membranes, leading to accelerated neuronal cell death and loss of synapses. Omega-3 fatty acids have been found to modify the microstructure of cell membranes, capturing tau aggregates within cells.
Researchers develop new method for selectively binding proteins to nanoparticles using co-assembling points of contact, promising applications in diagnostics and medicine. The method has potential for treating diseases such as Alzheimer's by dissolving amyloid aggregates.
A new transgenic rat model accumulates amyloid specifically in brain blood vessels, strongly mimicking human cerebral amyloid angiopathy. The rTg-DI rats exhibit progressive accumulation of brain blood vessel amyloid-associated inflammation, cognitive impairments, and microbleeds.
Researchers found that a pharmacological inhibitor of HDAC3 reduced amyloid-beta in vulnerable brain regions and improved memory in a transgenic mouse model of Alzheimer's disease. The study suggests that HDAC3 represents a potential drug target for several hallmarks of AD.
Researchers at University of Colorado Boulder found that amyloid-like structures play a beneficial role in the development of healthy muscle tissue during regeneration. The discovery sheds new light on potential origins of diseases such as ALS, inclusion body myopathy, and muscular dystrophy.
Scientists at the University of Leeds have used powerful microscopy techniques to reveal the structure of amyloid proteins, a build-up of abnormal proteins that causes disease. The research has provided significant insights into how these proteins form aggregates and contribute to disease, paving the way for potential treatments.
Researchers identified SynuClean-D as a potential therapeutic for neurodegeneration, which disrupts amyloid fibrils and inhibits alpha-synuclein aggregation. The compound reversed degeneration of dopaminergic neurons in animal models, offering hope for halting Parkinson's disease-related neurodegeneration.
Researchers propose using blood-brain barrier breakdown as an early warning sign for Alzheimer's disease, which could lead to earlier diagnosis and treatment. Healthy blood vessels are crucial for normal brain functioning, and damage can be detected with imaging tests such as MRI.
Researchers have devised a novel strategy to identify people with mild cognitive impairment at risk of developing Alzheimer's disease. The Loewenstein-Acevedo Scales for Semantic Interference and Learning (LASSI-L) tool measures specific memory deficits that align with imaging findings for abnormal brain amyloid accumulation.
Researchers at Washington University in St. Louis create 'blink' method to image amyloids, allowing for non-invasive visualization of these problematic proteins. The technique uses temporary fluorescence, causing amyloids to flash and enabling researchers to better understand their structure and behavior.
Tafamidis improves survival and quality of life, reducing hospitalizations in patients with transthyretin amyloid cardiomyopathy. The therapy delays neurologic progression in a similar condition, and has been approved for this condition in the EU.
A phase three clinical trial has shown that tafamidis can reduce deaths by 30% and cardiovascular-related hospitalizations by 32%. The treatment also slows the decline in quality of life among patients with transthyretin amyloid cardiomyopathy. If approved, it would be the first medical therapy for this life-threatening disease.
Researchers have developed tools to break down pesticides in the environment using catalytic amyloids. The discovery shows that these molecules can facilitate multiple chemical transformations at once, offering a promising approach for OP detoxification. Catalytic amyloids have been shown to hydrolyze paraoxon by several thousand-fold.
Scientists at TUM have discovered a new class of designed macrocyclic peptides that are highly potent inhibitors of amyloid formation, which could be an alternative to current antibody-based approaches. The researchers are now planning further investigations to verify their effectiveness in in vivo models.
BACE inhibitors may fail Alzheimer's trials due to impaired differentiation of newborn cells, according to a study published in eNeuro. The research suggests that partial BACE inhibition could represent an alternative strategy for reducing AD pathology while maintaining adult neurogenesis.
Meytal Landau is honored for her creative and committed work on amyloid-like fibers and alpha-helical structures. The Biophysical Society recognizes her contributions to advancing scientific knowledge and promoting diversity in researchers.
Researchers used proteomics to study the basic biology of Alzheimer's disease, cancer, and listeriosis. They found that BACE1 inhibition increases amyloid precursor protein and other substrates in Alzheimer's, while butyrate activates mitochondrial oxidation and suppresses tumor growth in colorectal cancer cells.
Researchers propose native state is a 'fortunate trap' that prevents spontaneous folding into fibril state, associated with Alzheimer's and Parkinson's diseases. The amyloid state is more stable thermodynamically, but kinetic barriers prevent its formation.