Articles tagged with Amyloids
A study suggests that aging HIV patients are at risk of developing dementia due to the accumulation of amyloid beta in their brains. Researchers found a correlation between years of infection and increased amyloid beta levels, suggesting that good clinical control of plasma HIV may not be enough to prevent related pathologies.
Dr. Li-Huei Tsai's groundbreaking study reveals p25 protein's role in Alzheimer's disease, a key feature of which is the presence of beta amyloid plaques and neurofibrillary tangles. The research also suggests an intervention after stroke could lower or prevent additional risk of Alzheimer's
Researchers found three to four times more antibodies in Alzheimer's patients than healthy individuals, indicating a possible autoimmunity component to the disease. This discovery may lead to an early diagnostic test and more targeted treatments.
Researchers discovered a protein that dissolves amyloid fibers in yeast cells, which could have implications for understanding protein folding processes and the role of environmental factors in evolution. The finding also sheds light on the natural biology of Sup35, a protein involved in genetic translation.
A study using mouse models of Alzheimer's disease found that blocking the Fyn enzyme reduces amyloid protein damage to synapses and improves longevity. However, increasing Fyn levels worsens synaptic damage and shortens lifespan. The findings suggest that pharmacological modulation of Fyn may be beneficial in treating Alzheimer's.
A study on transmissible spongiform encephalopathies (TSEs) and prion protein PrPSc accumulation in muscle tissue of infected rodents found that the defective form of PrPSc is present prior to clinical symptoms. The accumulation of PrPSc is greatest after clinical symptoms are well established.
Researchers found that increased expression of ADAM10 reduced AB peptide formation and prevented plaque formation in an Alzheimer disease mouse model. This suggests that targeting alpha-secretase might be a useful therapeutic target for AD.
Researchers identified a series of genes related to mitochondrial metabolism in brain cells that were more active in mice with Alzheimer's disease. These genes are thought to provide new insights into the disease's early cellular changes and may lead to the development of novel interventions.
Recent studies have identified key molecular markers of cognitive decline in Alzheimer's disease, revealing a complex role of amyloid proteins in the condition. These findings have significant implications for developing new treatments that target the underlying processes driving the disease.
Researchers isolate three strains of yeast prions that transmit life-changing information in yeast cells without DNA or RNA. These protein-only particles act like genes, disrupting normal cell function and leading to the formation of amyloid plaques associated with neurological disorders.
Researchers confirm that shape change accounts for strain differences in prions, laying groundwork for strategies to block disease. Prion shape underlies ability to jump between species, according to new finding.
A new animal model has been created to evaluate the effectiveness of an Alzheimer's vaccine, with promising results in clearing brain amyloid and reversing cognitive decline. The study involved vaccinating rhesus monkeys with beta-amyloid, a protein fragment suspected of disrupting nerve cells in the Alzheimer brain.
Scientists propose that alterations in cholesterol and ceramide contribute to neurodegenerative cascade destroying neurons in Alzheimer's disease. Oxidative stress triggered by beta amyloid peptide leads to ceramide accumulation, causing nerve cell death.
A new imaging agent, Pittsburgh Compound B, provides a unique view of amyloid plaques in the living human brain. This breakthrough discovery may contribute to understanding how Alzheimer's disease begins and grows, as well as develop effective treatments.
Researchers have found that a new vaccine can diminish symptoms of Alzheimer's disease by increasing clearance of amyloid beta protein from the brain. The study used monkeys and showed that vaccinating them with synthetic amyloid beta peptide enhanced clearance, leading to reduced plaques and improved cognitive function.
Researchers at Saint Louis University have identified a protein transport deficit as a key factor in Alzheimer's disease. The study suggests that reversing this deficit could lead to a new therapeutic target for treating the condition.
Researchers have found small, soluble aggregated proteins called ADDLs in the brains of individuals with Alzheimer's disease, up to 70 times more than in normal individuals. These proteins may be reversibly blocking memory function, providing a potential target for new therapeutic drugs.
Researchers found that meclofenamic acid and flurbiprofen, a currently clinical-trialled drug for prostate and colon cancer, effectively decreased Abeta42 levels by targeting gamma-secretase. This provides promising avenues for Alzheimer's treatment and furthers understanding of how NSAIDs impact AD.
Researchers found that caspase cleavage of tau promotes the formation of abnormal filaments resembling tangles. This discovery provides a new link between amyloid-beta and tau tangles, suggesting a common cause for Alzheimer's disease.
A study found that Alzheimer's disease alters a protein called calbindin in brain cells, leading to cognitive deficits. Calbindin levels in granule cells were strongly correlated with cognitive decline in genetically engineered mice and human patients.
Researchers identified a previously unknown protein family, chaplins A-H, essential for S. coelicolor's aerial hyphae formation. Exogenous application of chaplin proteins restores aerial growth in streptomycetes lacking specific genes.
Research reveals that amyloid accumulation selectively reduces expression of genes essential for forming new memories, leading to early memory loss in Alzheimer's disease. The study suggests a new approach to treating the disease by blocking the effect of remaining amyloid on normal learning and memory.
Researchers discover that Alzheimer's protein amyloid beta is transported into the brain by riding piggyback on a larger molecule called RAGE. This discovery opens up new possibilities for treating the disease. By blocking RAGE, blood flow to the brain can be restored and amyloid plaques reduced.
Emory University researchers have successfully self-assembled Alzheimer's amyloid fibrils into well-defined nanotubes. These nanotubes exhibit unique properties and can be used to build nanotechnological devices, offering new avenues for research and potential applications in fields such as medicine and materials science.
Researchers found that lithium significantly reduces production of beta amyloid, a key component of Alzheimer's disease. The study suggests that combination therapy with lithium and non-steroidal anti-inflammatory drugs may have an enhanced effect in reducing amyloid peptide accumulation.
Researchers are testing a new stroke prevention drug, NC-758, to determine its effectiveness in reducing amyloid angiopathy-related strokes. The trial aims to assess the drug's potential benefits for patients with Alzheimer's disease, which is characterized by excessive amyloid buildup.
A study published in Proceedings of the National Academy of Sciences found a relationship between insulysin and Alzheimer's disease. The researchers discovered that even partial decreases in insulysin activity raised amyloid-beta peptide levels in the brain, increasing the risk of Alzheimer's.
Researchers at Case Western Reserve University discovered molecules that play a critical role in triggering inflammation in the brain, which speeds up Alzheimer's disease progression. The study found that blocking these molecules' interaction with amyloid plaques could lead to a slower disease progression.
Researchers discovered that tau and alpha-synuclein proteins interact to form brain lesions in both diseases, potentially leading to effective treatments for both conditions. The study found that inhibiting the formation of one type of amyloid lesion may also prevent the other.
Researchers found that increasing neprilysin levels decreased amyloid deposition and reduced plaque load in transgenic mice. Astrocytes also degraded beta-amyloid peptides, suggesting a new target for AD therapies.
Researchers develop method to prevent amyloid formation by stabilizing the native state of proteins, preventing disease-associated subunits from contributing to fibril formation. This approach has potential therapeutic applications for various amyloid diseases, including familial amyloid polyneuropathy and cardiac disorders.
The Lancet Neurology recently published a series of articles discussing the latest evidence on Alzheimer's disease, including preventative anti-inflammatory clinical trials and the role of secretases in producing amyloid-beta peptide. Researchers argue that these approaches hold promise for preventing or slowing the onset of the disease.
Researchers found that beta-secretase activity is increased in Alzheimer's diseased brains, specifically in temporal and frontal cortex. This increase persists throughout the duration of the illness, making BACE a promising target for treatment, even late in the disease.
Researchers at Georgetown University Medical Center have discovered a key link between high cholesterol and the development of Alzheimer's disease. Elevated cholesterol levels increase the production of beta amyloid protein, leading to brain cell death and characteristic plaques found in Alzheimer's brains.
A new blood test was developed using a mouse model of Alzheimer's disease, which can detect amyloid plaques and predict dementia risk. The test uses a protein called Ab40, which is not reflective of brain pathology unless an antibody is injected into the animal.
Certain strains of E. coli produce amyloid fibers similar to those found in Alzheimer's disease, forming a meshwork around the bacteria in biofilms. This discovery raises questions about the role of bacterial infections in amyloid diseases, including Alzheimer's, and may lead to new treatment options.
Researchers have identified amyloid precursor protein (APP) as a key player in the molecular transportation system of the brain. The protein's cellular trafficking function is linked to the formation of harmful plaque deposits called amyloid beta, which are characteristic of Alzheimer's disease.
Researchers at Scripps Research Institute develop a therapy to prevent misfolding diseases by incorporating a protein suppressor into the diseased protein, stabilizing it and preventing fibril formation. This approach may also work for other diseases with similar protein-protein interactions.
A new double transgenic mouse model has been developed to study Alzheimer's disease, featuring both brain plaques and tangles associated with the condition. The model is expected to contribute significantly to knowledge about the course of the disease and aid in further development and testing of potential therapies.
Researchers at Mayo Clinic have successfully bred mice with both amyloid plaques and neurofibrillary tangles, the key pathologic hallmarks of Alzheimer's disease. The double transgenic mouse model provides a more complete representation of human AD and will enable researchers to test therapies aimed at preventing or halting progression.
Researchers at NYU Langone Health successfully immunized mice against Alzheimer's disease using a new vaccine that reduces amyloid plaque and soluble beta levels. The vaccine, modeled on a modified peptide, appears to be non-toxic and shows great promise for the treatment of Alzheimer's disease.
Researchers at WashU Medicine discovered an antibody that targets a specific region of the amyloid-beta protein, drawing it out of the brain and into the blood. The study found that mice treated with the antibody developed fewer amyloid plaques in their brains than control animals.
Researchers analyze kinetics of amyloid b1-40 peptide clearance in mice brains, finding vascular transport is primary mechanism. They also suggest ApoE plays role in amyloid clearance pathway.
Scientists at Johns Hopkins have identified a specific enzyme, beta-secretase, as crucial for forming the hallmark amyloid plaques of Alzheimer's disease. The study, which used mice models, suggests that targeting this enzyme could offer new therapeutic options for treating the condition.
The World Alzheimer Congress will showcase recent discoveries on Alzheimer's disease, including the link between cell suicide and amyloid protein accumulation. Researchers also explored the role of apoE4 in driving brain damage and cognitive decline.
Researchers at the University of Pennsylvania School of Medicine have created a stealth-like molecule called BSB that can effectively breach the blood-brain barrier and bind to amyloid plaques, enabling visualization using PET or SPECT imaging. This breakthrough paves the way for the refinement of BSB as a diagnostic tool for Alzheimer...
Researchers at the University of Kentucky have discovered a new potential target for compounds that may treat or prevent Alzheimer's disease. The receptor RAGE interacts with amyloid fibrils, accelerating fibril formation and inducing cellular dysfunction.
Researchers discovered a molecule, ERAB, that causes early neuron damage in Alzheimer's disease. The finding may lead to therapies that inhibit the interaction of ERAB and amyloid-B peptide, protecting neurons from damage.