Articles tagged with Amyloids
Researchers have identified a subset of neurons in the mammillary body that are most susceptible to neurodegeneration and hyperactivity in Alzheimer's disease. These findings suggest that this region may contribute to early symptoms of the disease, making it a potential target for new drugs.
Researchers developed a new imaging technique that visualizes the interaction between reactive astrocytes and neurons in the brain, revealing a potential breakthrough in Alzheimer's disease diagnosis and treatment. The study found that acetate promotes reactive astrogliosis, leading to dementia, and offers a new target for AD treatment.
Research by Whitehead et al. reveals that cellular senescence triggers amyloidosis through changes in small extracellular vesicles and extracellular matrix composition. The study provides novel insights into the formation of aortic medial amyloid and offers potential therapeutic targets for mitigating its effects.
Researchers used a novel brain imaging technique to visualize subtle brain changes in pre-symptomatic Alzheimer's patients. They found that individualized brain fingerprints can detect variations in brain function associated with worsening information processing.
Researchers at NTU Singapore have found a way to spur brain immune cells to clear toxic waste linked to Alzheimer’s disease by targeting their metabolism. The study reveals a ‘metabolic switch’ in the brain’s immune cells that can be manipulated to improve their function.
Reducing mRNA methylation promotes migration of macrophages into the brain and clearance of toxic protein amyloid-beta. This pathway provides a potential new target for treatment of Alzheimer's disease.
Researchers found that platelet depletion increased amyloid plaque size and neuronal damage in APP-PS1 mice. However, platelets may have a beneficial role in limiting plaque growth and attenuating neuritic dystrophy at advanced stages of Alzheimer's disease.
Researchers at Universitat Autonoma de Barcelona solved the structure of a functional amyloid protein, hnRNPDL-2, which forms stable and non-toxic fibres in humans. The discovery changes the concept of disease origin and treatment, suggesting that molecules stabilising or facilitating fibre formation could be the key to therapy.
Researchers identified an alternative binding site on amyloid-beta aggregates using time-resolved spectroscopy and computational chemistry. This discovery could lead to the development of new therapies for Alzheimer's disease and other conditions associated with amyloid deposits.
Researchers have developed a novel blood-based biomarker, brain-derived tau (BD-tau), that specifically measures non-phosphorylated tau originating from the brain. This breakthrough addresses an unmet need for a blood test that tracks neurodegenerative changes in Alzheimer's disease but not in other dementias.
A new USC study found that the buildup of amyloid beta protein in the brain is not directly linked to Alzheimer's disease, but rather a general change associated with aging. Researchers discovered higher levels of soluble Aβ protein in healthy brains, while insoluble fibrillary amyloid was more closely tied to poor brain health.
A new laboratory test can measure levels of amyloid beta oligomers in blood samples, detecting toxic proteins up to years before cognitive impairment. The test, SOBA, has shown promising results in identifying individuals at risk or incubating Alzheimer's disease.
A novel peptide has been developed to selectively detect and neutralize an early molecular trigger of Alzheimer's disease. The technology allows for the detection of the disease at all stages, including presymptomatic cases, with high sensitivity and specificity.
Researchers identify INPP5D as a key player in the inflammation process contributing to Alzheimer's disease, which may offer new potential targets for therapies. The study found that mice with inactivated INPP5D gene had more plaques covered by microglia, suggesting unexpected results when modulating inflammation genes.
A new study published in the journal Nature has identified medin as a key player in Alzheimer's therapies. Medin, a protein that accumulates in the blood vessels of the brain, promotes vascular pathology and cognitive decline. The researchers hope to develop a treatment targeting medin to prevent vascular damage and cognitive decline.
A recent study reveals that Down syndrome brains develop the same amyloid beta and tau prions as Alzheimer's disease, causing neurological dysfunction. With over 50% of people with Down syndrome developing Alzheimer's by age 40, this discovery offers new insights into the common underlying causes of these two diseases.
The FDA approved Aduhelm for Alzheimer's treatment based on reduced amyloid levels in the brain, despite no significant clinical effect. The use of amyloid-PET scans is being questioned for its accuracy and reliability in measuring amyloid removal.
Researchers at Lund University have discovered that people with Alzheimer's disease can be identified before symptoms appear, using PET scans to visualize tau and amyloid proteins in the brain. Participants found to have these biomarkers were at a 20-40 times higher risk of developing cognitive decline in the next few years.
Researchers at Technical University of Munich developed synthetic peptides that bind to proteins forming amyloids, preventing their aggregation. These peptides could be valuable candidates for treating both diseases, with potential for medical application.
Researchers found that extracts from hop flowers can inhibit the clumping of amyloid beta proteins, associated with Alzheimer's disease. The Tettnang hop extract showed potent anti-aggregation and antioxidant properties, promoting the body's ability to clear out misfolded proteins.
Researchers evaluated the safety and efficacy of NTLA-2001 in patients with transthyretin amyloid cardiomyopathy. The results showed significant reductions in circulating TTR protein levels, which were sustained for up to six months after treatment.
A new radiotracer, 18F-SMBT-1, detects overexpressed monoamine oxidase-B in cognitively unimpaired individuals with high beta amyloid levels, a key early sign of Alzheimer's disease. The agent shows increased binding to reactive astrocytes, suggesting its potential as a surrogate marker for detecting Alzheimer's disease.
Researchers from Osaka University found that serum albumin can prevent the formation of amyloid fibrils in dialysis patients by interfering with β2m protein clumping. Monitoring serum albumin levels may help predict and delay the onset of dialysis-related amyloidosis, a condition also linked to Alzheimer's disease.
Researchers from the University of Cincinnati found that low levels of soluble amyloid-beta protein in the brain, rather than its buildup into plaques, are associated with cognitive decline and Alzheimer's disease. Patients with high levels of soluble amyloid-beta showed improved cognitive outcomes, contradicting previous theories.
The Keck School of Medicine of USC's Stevens INI has received a $149 million grant to study Alzheimer’s disease among diverse communities. The HABS-HD study aims to develop biomarkers that determine risk for developing the disease, addressing health disparities among Hispanic and African American populations.
A new study found that fewer Asian, Black, and Hispanic patients qualify for anti-amyloid monoclonal antibody treatments, which may slow Alzheimer's progression. The treatment's effectiveness depends on the presence of amyloid plaques, with lower incidence in minorities.
Scientists at UCLA discovered several molecules that can destroy tau fibers, long filaments thought to cause Alzheimer’s and similar diseases. The green tea molecule EGCG helped identify these molecules, which could lead to new treatments for Alzheimer’s and related conditions.
Researchers developed a novel way to visualize densely packed molecules using expansion microscopy, allowing for the first time their imaging. The technique enables visualization of nanostructures found in neurons and Alzheimer's-linked amyloid beta plaques.
Researchers at Washington University School of Medicine have discovered a new pathway that could help prevent Alzheimer's dementia. Increasing the clearance of waste products in the brain by ramping up a genetic quirk known as readthrough may be effective for other neurodegenerative diseases, such as Parkinson's disease.
This special collection of articles explores the 'dark side' of Alzheimer's Disease, revealing new biomarkers for brain hyperexcitability and its impact on vigilance and sleep-wake cycle. The findings provide a foundation for an extended model to speed up research lines and discovery.
Researchers found higher levels of brain cell damage and inflammation markers in women with severe preeclampsia compared to those with uncomplicated pregnancies. The study used health record data from the Rochester Epidemiology Project and explored extracellular vesicles as potential early risk indicators.
A KAIST research team has discovered a new role for somatostatin, a protein-based neurotransmitter, in reducing the toxicity caused by Alzheimers disease. When somatostatin is met with copper and Aβ proteins, it attenuates the toxicity and agglomeration of metal-Aβ complexes.
A new advanced MRI technique has enabled clinicians to measure the effectiveness of chemotherapy in patients with stiff heart syndrome, improving their prognosis. By accurately measuring amyloid protein deposits in the heart, doctors can better guide treatment strategies and improve patient outcomes.
A new study demonstrates that glyphosate successfully crosses the blood-brain barrier and enhances TNF-α levels in mice. The herbicide is linked to increased production of soluble beta amyloid and reduced neuron viability, suggesting potential hazards to neurological health.
A recent PLOS Biology study examines the limitations of current anti-amyloid therapies for Alzheimer's disease, suggesting abnormal microglial function and tau tangles as key mechanisms. The authors review clinical trial results and propose new strategies for treating the disease, bringing hope for a cure.
Researchers found reduced levels of Histone Deacetylase I (HDAC I) in the brains of patients with Alzheimer's disease, linked to deleterious effects of misfolded beta-amyloid and tau proteins. HDAC inhibitors, currently being tested against mild Alzheimer's disease, may be harming patients rather than helping them.
A new study from UTHealth Houston found that whole blood exchange treatments decreased amyloid plaque formation in mice with Alzheimer's disease-causing amyloid precursor proteins. This approach has the advantage of treating the disease in the circulation instead of the brain, potentially bypassing the blood-brain barrier.
A study published by researchers at the University of Colorado Anschutz Medical Campus found that psychiatric drugs imipramine and olanzapine can improve symptoms of Alzheimer's disease, including boosting cognition and reversing clinical diagnoses.
A new UCLA study found that fixed vial sizes for the controversial Alzheimer's drug aducanumab could result in significant wasteful spending of up to $605 million per year on Medicare. The researchers suggest reducing vial sizes to contain costs and improve the value of future Medicare spending.
Scientists have created a membrane made from a waste by-product of vegetable oil manufacturing that can filter out heavy metals from contaminated water. The membrane uses proteins derived from peanut or sunflower oil production to attract and trap heavy metal ions, purifying water to international drinking standards.
Researchers discovered a link between the astrocytic urea cycle and Alzheimer's disease memory loss. The study found that the urea cycle helps clean up toxic amyloid-beta aggregates, but its activation also causes the production of harmful byproducts, leading to neuronal death.
Researchers have developed a new probe to detect Alzheimer's disease biomarkers using near-infrared fluorescence, which may help diagnose the disease early and prevent its progression. The probe binds oligomeric Aβ proteins, a hallmark of Alzheimer's disease, offering a potential alternative to existing treatments.
Researchers will track changes in the blood-brain barrier, neurovascular function, and cognition in over 850 participants with genetic variants at risk of developing Alzheimer’s disease. The study aims to improve understanding of the onset and progression of Alzheimer’s disease and identify effective interventions.
Researchers found that neuronal damage in Alzheimer's disease originates from within brain cells' lysosomes, where amyloid beta appears. This discovery could explain why drugs designed to remove amyloid deposits have failed to stop the disease.
The JNM Molecular Imaging of Neurodegeneration Supplement provides an overview of molecular imaging techniques in neurodegenerative disorders. The supplement aims to improve early and differential diagnosis, as well as stratify and monitor therapy in these disorders.
Alzheimer's disease causes cells to overheat due to amyloid-beta aggregation, which can lead to more aggregates forming. The researchers found a drug compound could stop this process, potentially leading to new treatments.
Scientists found a connection between the SARS-CoV-2 virus and the production of misfolded proteins called amyloids, which can cause complex symptoms and damage in organs such as the heart and kidneys. The researchers' discovery may help explain why COVID-19 often affects multiple parts of the body.
Researchers discovered a strong link between subjective cognitive impairments and elevated beta-amyloid protein levels, indicating early-stage Alzheimer's disease. The study suggests that combining these two factors can help identify individuals at risk for developing dementia.
Researchers used PET and fMRI to study brain connectivity changes years before symptoms of Alzheimer's disease appear. Disruptions were found in the main memory network, even before cognitive impairment was observed, suggesting potential strategies for early detection.
A team at Baylor College of Medicine found that human NANOG's 'super stickiness' enables it to form large aggregates at low concentrations, which interact with chromatin to activate a pluripotent state. This process involves reshaping the genomic landscape and turning on genes involved in pluripotency.
Research suggests that EMFs can cause Alzheimer's disease by building up calcium levels in brain cells. This increase leads to changes in the brain, which develop conditions for Alzheimer's. The study highlights the importance of reducing EMF exposure to prevent or delay the onset of Alzheimer's.
Researchers at UCLA have discovered that amyloid fibrils in the brains of patients with frontotemporal degeneration are composed of the protein TMEM106B, not TDP-43 as expected. This finding may lead to new focus on TMEM106B in FTLD and similar brain diseases.
Researchers found a clear link between elevated amyloid beta levels and the development of anxiety and apathy in Alzheimer's patients. These symptoms occur mainly due to underlying brain changes, not psychological reactions. The study suggests that psychiatric symptoms could be used as alternative outcome measures in treatment trials.
Researchers found a higher number of small HDL particles in cerebrospinal fluid is associated with better cognitive performance and lower risk for Alzheimer's disease. These particles may play a key role in clearing amyloid beta peptides, which contribute to the disease.
Researchers found that high levels of both amyloid and tau proteins impair memory functions, but only when amyloid burden is also high. The study suggests that anti-amyloid therapies may be beneficial in reducing memory impairment in the early stages of Alzheimer's disease.
A new study identifies the age-dependent formation of TMEM106B amyloid filaments in human brains, which may not be linked to neurodegenerative diseases. Researchers found these protein structures in older but not younger individuals, suggesting a potential role in aging and other pathologies.
Researchers at Lewis Katz School of Medicine identify reduced efficiency of protein transport system as key factor in Alzheimer-like changes. The study suggests that targeting the retromer complex could lead to new treatments for Down syndrome-related dementia.
Researchers identified peripheral tissues as source of blood amyloid beta, which regulates blood glucose levels and suppresses insulin secretion. The study suggests a possible mechanism linking type 2 diabetes to Alzheimer's disease development.
A new blood test developed at Washington University School of Medicine has proven highly accurate in detecting early signs of Alzheimer’s disease, with a 93% accuracy rate. The test assesses amyloid plaques based on the ratio of A´2 and A´0 proteins in the blood, providing a low-cost alternative to expensive brain scans and spinal taps.
Researchers developed a vortex microscope that captures detailed motion and rotation of molecules in liquid. The technique provides unprecedented insight into molecular dynamics, enabling the study of diseases like Alzheimer's.