Articles tagged with Amyloids
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The new molecules are formed by a chain of 7 amino acids, each composed of only two different amino acids. These peptides have numerous applications, including generating electrical nanoconductors and fibrillar mini enzymes capable of acting as catalysts in the formation of organic nanomaterials.
Exosomes in brains affected by Alzheimer's disease contain toxic aggregates of amyloid beta and tau proteins, spreading the disease to new neurons. The study opens up the possibility of diagnosing Alzheimer's disease and developing drugs that could prevent the spreading.
Amyloid peptides prevent CamKII from participating in synaptic plasticity, leading to synapse loss and cognitive deficiencies. Researchers aim to understand the molecular mechanism behind amyloid aggregate interactions with CamKII to develop potential treatments for early Alzheimer's disease.
Research reveals that alcohol impairs microglial cells' ability to clear amyloid beta, contributing to Alzheimer's disease development. The study found altered gene expression for 312 genes under alcohol exposure.
Researchers found that APOE4 promotes beta amyloid protein accumulation, leading to Alzheimer's pathology. They also discovered that editing the gene can eliminate signs of Alzheimer's in brain cells.
Researchers have discovered that a compound found in green tea can break up potentially dangerous protein plaques in the blood vessels, which can reduce the flow of blood to the heart and brain. This discovery could lead to new medicines to treat heart attack and stroke.
A research group has developed a new technique to study the behavior of p53 conformers, which are prone to forming amyloid aggregates that contribute to cancer development. The approach allows researchers to observe these conformers before they aggregate, providing potential tools for understanding and blocking their formation.
Researchers found that combined vascular risk factors and high brain amyloid levels predict faster cognitive decline in clinically normal older individuals. Vascular risk remained a strong predictor of cognitive decline even when controlling for other biomarkers.
Researchers have identified a mutation that can reduce amyloid-beta plaque accumulation in mice, a hallmark of Alzheimer's disease. The study found that mice with the mutated APP gene had less amyloid-beta build-up, suggesting a potential therapeutic target.
Researchers used a powerful X-ray laser to analyze amyloid proteins, which are linked to neurodegenerative diseases like Alzheimer's. The new method allows for detailed structural analysis of individual amyloid fibrils, enabling scientists to better understand their role in disease development.
Researchers found that brain cholesterol triggers amyloid-beta protein clusters, a key player in Alzheimer's disease. The study suggests targeting cholesterol regulation as a potential treatment approach.
Researchers have created a rat model that can be used to study the buildup of amyloid plaques and vascular abnormalities in the brain, two key traits of Alzheimer's disease. The model, which uses human APP and PS1 proteins, has shown poor memory and learning in rats, similar to those observed in humans suffering from Alzheimer's.
Researchers from Chalmers University of Technology have discovered that a protein called parvalbumin, found in many fish species, can form amyloid structures that bind to and neutralize the 'Parkinson's protein' alpha-synuclein. This could potentially help prevent the formation of harmful amyloids associated with Parkinson's disease, a...
Researchers found that combining two approaches to reduce amyloid-beta improved spatial navigation and memory in a mouse model of Alzheimer's disease. The study suggests similar combination treatments may help patients with Alzheimer's disease in the future.
A study led by researchers at Linköping University found that amyloid beta, a protein linked to Alzheimer's disease, has different properties in different cell types. Glial cells can produce mature, less harmful forms of the protein, while neurons are more susceptible to damage.
Researchers at McGovern Medical School are studying how protein deposits in the brain can trigger dementia and stroke. Akihiko Urayama's team is examining the brain's clearance system, while Louise McCullough's team is investigating the gut-brain connection.
Researchers discovered that the apoE4 gene causes damage in human brain cells by altering its main structure and function. They found that adding a small molecule structure corrector eliminates signs of Alzheimer's disease, restores normal cell function, and improves survival in human apoE4 neurons.
A new blood test has been developed to detect early indicators of Alzheimer's disease, measuring the relative amounts of pathological and healthy amyloid-beta forms in the blood. The test was found to reliably detect signs of the disease on average eight years before diagnosis, with an overall diagnostic accuracy of 86%.
Researchers at WashU Medicine have developed an antibody that targets APOE protein, leading to the removal of amyloid plaques from mouse brains. This breakthrough could potentially halt brain damage triggered by plaques in early stages of Alzheimer's disease.
Researchers at WashU Medicine found a direct correlation between amyloid plaques and tau protein production in the brain. Targeting tau production may lead to new treatments for Alzheimer's disease.
A new biocompatible catalyst selectively oxygenates and degrades amyloid-β peptide under near-infrared light irradiation, reducing its pathogenic properties. The catalyst is applicable for treating peripheral amyloid diseases and Alzheimer's disease.
Researchers discover TREM2 receptor mediates anti-amyloid toxicity, potentially preventing or reducing neurodegenerative disorders like Alzheimer's. Boosting TREM2 levels in the brain may prevent disease progression and restore cognitive function.
Four neuroscientists, including Christian Haass, receive the Brain Prize for their work on the genetic and molecular bases of Alzheimer's disease. Their research has revolutionised understanding of the changes in the brain that lead to Alzheimer's, with potential implications for diagnosis, treatment, and prevention.
Researchers found that a compound enhanced protein trafficking reduced amyloid beta and Tau protein production in brain cells. The study suggests targeting endosomal network defects as a promising strategy against Alzheimer's disease.
Researchers at ETH Zurich have made a groundbreaking discovery that protein amyloids can self-replicate, challenging the long-held RNA hypothesis as the origin of life. The findings suggest that early life forms may have used amyloids as information carriers and catalytic units.
A Canadian study found that individuals close to their parent's onset age of Alzheimer's are more likely to have amyloid plaques in their brain. The research also suggests a stronger link between parental age, ApoE4 gene carriers, and increased disease risk.
A new data analysis of 51 existing studies in mice reveals that phosphorylated tau (p-tau) is a more likely culprit in Alzheimer's disease than previously thought. The study also found that multiple biochemical actors work together to tear down neurons, and that soluble amyloid-beta has a strong correlation with cognitive decline.
A new study challenges the long-held assumption that amyloid beta buildup in brain cells is the origin of Alzheimer's disease. Researchers found that standard diagnostic tools fail to detect future AD in many patients under age 70, and that a decline in cerebrospinal fluid clearance may be the early feature of AD.
A new study reveals that people with preclinical Alzheimer's disease experience significant disruptions in their internal body clocks, even after controlling for other factors. These circadian rhythm disruptions are linked to increased risk of developing the disorder and may serve as a biomarker for early detection.
A large clinical trial found that solanezumab, a monoclonal antibody-based treatment for Alzheimer's disease, did not significantly slow cognitive decline. Researchers propose alternative strategies and ongoing studies may lead to effective treatments.
Researchers find that beta amyloid protein disrupts mitochondria function, leading to early disease symptoms. Human cells can be protected from damage with a custom-designed compound, offering an exciting avenue for future drug development.
Researchers analyze brain slices from patients with Alzheimer's and cerebral amyloid angiopathy, finding distinct amyloid-beta prion strains associated with different disease types. Mutant amyloid-beta adopts self-propagating prion structure, imparting pathological conformation to normal amyloid-beta.
Researchers at Hong Kong Baptist University have invented multifunctional cyanine compounds that can be used for detection, imaging and treatment of Alzheimer's disease. The discovery has been granted US patents and a Chinese patent.
Researchers have developed small shining molecules that can recognize specific proteins in the brain, such as amyloid beta and tau. These molecules emit light at different wavelengths when bound to their target protein, enabling potential diagnostic tools for neurodegenerative diseases.
Researchers propose a new term, mapranosis, to describe the interaction between gut microbiota and brain proteins that contributes to neurodegenerative diseases. The process involves amyloid protein misfolding and inflammation in the nervous system.
A study by Temple University researchers found that mice fed canola oil daily suffered impaired working memory and increased amyloid plaques, indicative of neuronal damage. The findings suggest that long-term consumption of canola oil may be detrimental to brain health.
Researchers discovered that enhancing mitochondrial defenses can reduce amyloid plaque formation and improve cognitive function in Alzheimer's disease. The approach targets the mitochondrial unfolded protein response and mitophagy mechanisms to restore cellular energy production and protect against neurodegeneration.
A new PET tracer has been developed to effectively gauge the effectiveness of promising Alzheimer's treatments in mouse models. The tracer binds to BACE1, a key enzyme involved in amyloid-β development, and accurately measures its effects on brain metabolism, neuroinflammation, and amyloid-β pathology.
Researchers identified a compound targeting APOE protein in mouse brains, reducing amyloid beta plaques and neurological damage. The findings suggest APOE could be a potential target for treatment or prevention of Alzheimer's disease.
Researchers have discovered a small-molecule drug that can restore brain function and memory in mice with Alzheimer's-like symptoms by blocking toxic ion flow. The drug, anle138b, attaches to amyloid-beta protein clusters and deactivates pores, reducing neuronal dysfunction and cell death.
A new algorithm can speed up protein-folding simulations, allowing researchers to model phenomena that were previously out of reach. This technique can help scientists better understand and treat diseases like Alzheimer's, which is associated with amyloid-beta protein fragments forming hard plaques that disrupt neurons.
An international team of experts has made a fundamental discovery by transforming amyloid fibrils into crystals, a process previously thought to be impossible. The transformation involves untwisting the fibril to form an elongated, matchstick-like crystal with unprecedented stability.
Researchers at Sanford Burnham Prebys Medical Discovery Institute identified a new protective function for the brain protein SORLA, which limits amyloid beta's toxic signaling. The study suggests that increasing levels of SORLA in mice reduced cognitive impairments caused by amyloid beta.
A neuroprotective compound has been shown to protect against nerve cell death, depression, and memory problems in a rat model of Alzheimer's disease. The treatment also prevented the development of depression-like behavior and delayed cognitive decline.
Research suggests that amyloid-beta, a toxic protein, can travel to the brain from other parts of the body, contributing to Alzheimer's disease. This discovery offers hope for new drug therapies that target the kidneys or liver to prevent the protein from reaching the brain.
A probe invented at Rice University has identified a specific binding site on the amyloid beta peptide, which is suspected to cause Alzheimer's disease. This discovery could lead to the development of photodynamic therapy for Alzheimer's disease.
A study from the University of Pennsylvania sheds light on how seniors cope with results showing an elevated level of beta amyloid protein plaques, a biomarker of Alzheimer's-disease. Researchers found that many seniors are dissatisfied with the ambiguity of the message and desire more detailed information about their risk.
Rice University researchers have identified a specific binding site on the amyloid beta peptide, which could facilitate the development of better drugs to treat Alzheimer's disease. The probe uses light activation to catalyze oxidation of the protein, preventing it from aggregating in the brains of patients.
Scientists have characterized a new class of drugs that precisely block the production of toxic forms of beta-amyloid, a primary driver of Alzheimer's disease. Treatment with these gamma-secretase modulators reduces levels of amyloid-beta 42 in animal models and cellular systems.
Researchers found that high-risk TREM2 variants can hobble the immune system's ability to protect against amyloid beta, but later in the disease, the absence of TREM2 protein protects the brain from damage. The study suggests targeting the TREM2 protein as a means of preventing or treating Alzheimer's may be complicated and that doctor...
A computer model developed by InSysBio scientists suggests that activating beta-amyloid degradation is key to preventing protein plaques in the brain. The model found that starting treatment at age 60 can lead to relative normalization of indices, highlighting the importance of early intervention.
Researchers at Scripps Research Institute (TSRI) have developed a peptide probe that can detect non-native TTR oligomers, potentially leading to early diagnosis and treatment of amyloid diseases. The study revealed higher levels of non-native TTR oligomers in patients with TTR amyloid polyneuropathy.
Researchers developed an algorithm using AI and big data to recognize dementia signatures two years before onset from a single amyloid PET scan. The tool could improve patient care and accelerate treatment research into Alzheimer's disease.
Researchers found that impaired lysosome transport contributes to protein aggregate buildup in brains of mice with Alzheimer's. Developing ways to restore lysosome transport could represent a new therapeutic approach.
Researchers from Kent State University have identified pathologic hallmarks of Alzheimer's disease in the brains of aged chimpanzees, similar to human Alzheimer's disease brain pathology. The study found amyloid beta plaques and blood vessels in all 20 aged chimpanzee brains, with increasing sizes correlating to age.
A new BACE inhibitor has shown promise in improving brain function and memory performance in a mouse model of Alzheimer's disease. The study found that the treatment reduced amyloid beta production, restored normal nerve cell function, and improved memory abilities.
Researchers have discovered molecular basis of hereditary Alzheimer's disease, revealing a crucial role in the cleavage process of APP protein. Stabilizing Gamma Secretase-APP interaction may prevent release of toxic amyloid beta fragments, delaying or preventing the disease.
Researchers at Boston University School of Medicine have discovered how acidic conditions trigger the formation of toxic protein clusters in cells, leading to the death of vital organs. The study may help design new treatments for secondary systemic amyloidosis (AA), a life-threatening disorder that affects millions worldwide.
Researchers have developed a blood test that can detect amyloid beta plaques in the brain, a key characteristic of Alzheimer's disease. The test measures levels of three different amyloid subtypes and has been shown to be highly accurate in identifying individuals with altered levels of amyloid in their brains.
Researchers at the University of British Columbia have found that changing where an enzyme cuts a protein precursor can reduce amyloid beta plaque buildup, a key factor in Alzheimer's disease. By guiding the enzyme to a different point, the researchers may be able to achieve the same goal with less collateral damage.