Articles tagged with Amyloids
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A recent study by Mass General Brigham researchers found that adults with a family history of Alzheimer's disease on their mother's side had higher amyloid levels in their brains. This suggests that maternal inheritance may play a role in identifying individuals at heightened risk for developing the disease.
Researchers found that boosting mitochondrial health can combat protein clumping linked to both aging and Alzheimer's. The study identifies a core insoluble proteome enriched with numerous proteins not previously considered, offering new targets for exploration.
A new imaging technique developed by researchers at Washington University in St. Louis has allowed scientists to visualize the differences between synthetic peptides and amyloid beta fibril assemblies. The study provides valuable information on the heterogeneity of these assemblies, which is crucial for understanding protein toxicity a...
Researchers found that individuals from certain racial and ethnic groups are less likely to be eligible for Alzheimer's disease clinical trials due to lower amyloid levels at early stages of the disease. Amyloid buildup in the brain varies across different populations, contributing to underrepresentation in clinical trials.
Researchers investigate how early-stage Alzheimer's disease affects memory formation by examining synaptic connections and amyloid beta. The study aims to understand the role of NMDA receptors in synaptic plasticity and how they might be hijacked by amyloid beta, leading to memory dysfunction.
A Rice University research project aims to provide new insights into biological fibrillar nanostructures with potential implications for the treatment and diagnosis of Alzheimer’s and Parkinson’s diseases.
Researchers successfully transmitted familial Alzheimer's disease to normal lab mice through bone marrow stem cell transplant. The recipients developed cognitive decline and amyloid buildup at an accelerated rate, highlighting the systemic nature of Alzheimer's disease.
A study using a xenotransplantation model has revealed that human microglia respond to amyloid-β plaques with a complex immune response, influencing the disease course. The research highlights the importance of considering genetic factors in microglia-targeted therapies for Alzheimer's disease.
A study published by the University of Florida suggests a connection between elevated amyloid blood levels and subtle brain microstructural changes in individuals without dementia. Researchers used diffusion MRI to detect free-water in the brain, revealing associations with structural abnormalities even when PET scans were negative.
A new blood test has been shown to diagnose Alzheimer's disease pathology as accurately as FDA-approved spinal fluid tests, making early diagnosis and treatment accessible to more people. The blood test measures levels of Alzheimer's proteins in the blood, detecting molecular signs of the disease even before symptoms appear.
Scientists have discovered that inhibiting the Mdm2 protein can prevent the destruction of synapses and dendritic spines in Alzheimer's disease. This breakthrough could lead to a new approach for treating the disease, which may be more effective than current anti-amyloid therapies.
Researchers found GV1001 decreases BACE and Aβ1-42 levels, reducing neurodegeneration and senescence in 3xTg-AD mice. It also increases survival, telomere length, and telomerase activity, contributing to improved lifespan.
Post-translational modifications on alpha-synuclein slow amyloid aggregation and protect neurons, potentially slowing disease progression. The study's findings suggest that targeting these modifications could lead to new treatments for Parkinson's disease.
Researchers found that APOE4 accumulates on fat droplets in astrocytes, damaging brain cells and preventing them from cleaning up toxic lipids. This mechanism could explain why APOE4 increases Alzheimer's disease risk.
A team of scientists from the Beckman Institute has received a $3 million grant to develop diagnostic tools and imaging agents for the early detection of Alzheimer's disease. They will use a combination of PET and MRI scans to target smaller beta-amyloid peptides and other signs of neuroinflammation and oxidative stress.
Researchers have developed a fluorescent sensor array that can detect Alzheimer's-related proteins, allowing for earlier disease detection. The tool uses an array of sensor molecules that light up amyloids, providing a high level of sensitivity and selectivity in distinguishing between different amyloid-related conditions.
Researchers have identified five cases of Alzheimer's disease acquired through exposure to contaminated cadaver-derived human growth hormone (c-hGH) used in medical treatment between 1959 and 1985. Biomarker analyses and autopsy results confirmed the diagnoses, highlighting a rare but significant risk of transmission via this route.
Researchers at Northwestern University have discovered that toxic short RNAs contribute to neuron death and DNA damage in Alzheimer's disease. Studies found that older individuals with superior memories have higher amounts of protective short RNA strands in their brains.
Dutch scientists identified five distinct biological variants of Alzheimer's disease through cerebrospinal fluid proteomics. These variants differ in protein production, immune system function and nerve cell growth, affecting disease progression and treatment responses.
Researchers at HKUST have developed an optical plasmonic tweezer-controlled SERS platform to detect pH-dependent amylin species, revealing the secrets behind amyloid aggregation mechanisms. The platform enables efficient and high-throughput single-molecule characterization of various amylin species.
A study by Mass General Brigham found that daily learning tests can detect Alzheimer's disease-related changes in memory among cognitively normal older adults. The test, called BRANCH, was completed over seven days on a smartphone, revealing diminished learning curves associated with elevated amyloid levels.
A protein called TAF15 forms amyloid filaments in brain cells, affecting frontal and temporal lobes. This discovery identifies a potential target for diagnostic and therapeutic strategies for frontotemporal dementia.
Amyloids have been found to selectively bind with codon-sized RNA, a crucial step in the emergence of life. These interactions may represent a universal genetic code that unites all living beings, increasing stability and order in an otherwise dilute system.
Researchers developed a handheld, wireless biosensor to detect Alzheimer's and Parkinson's biomarkers from saliva and urine samples. The device has shown high accuracy comparable to existing state-of-the-art methods.
Scientists identify pyroglutamination, a spontaneous chemical change, in peptide synthesis, leading to an amyloidal structure and potential implications for neurodegenerative diseases like Alzheimer's and Parkinson's. The process favors aggregation of molecules, forming plaques that interrupt neuronal flow.
A new trial combining an Alzheimer's medication with two other drugs may amplify its effects and arrest disease progression. The trial, funded by a $150M grant, will recruit 900 participants with early-onset Alzheimer's.
Researchers at Chalmers University of Technology have shown that graphene oxide nanoflakes can reduce the accumulation of misfolded amyloid peptides in yeast cells, which are similar to human neurons affected by Alzheimer's disease. This suggests that graphene oxide may hold great potential for treating neurodegenerative diseases.
UAB researchers have designed minimal nanozymes with the capacity to capture carbon dioxide, applicable for environmental remediation and biotechnology research. These new molecules are formed by peptides of only seven amino acids and can act as metalloenzymes, opening up possibilities in extreme temperatures and pH values.
Researchers at Tokyo Medical and Dental University found that mutant α-synuclein protein propagates through the brain's lymphatic system in its monomeric state before aggregating, shedding light on Parkinson's disease progression. The study suggests targeting early events may limit disease progression.
A new blood-based test called p-tau217 has shown great promise in identifying Alzheimer's disease by stratifying patients into low, intermediate, and high-risk groups. The two-step workflow reduces the need for confirmatory testing in uncertain cases.
A new article published in RadioGraphics warns of a potential side effect of novel Alzheimer's treatments: amyloid-related imaging abnormalities (ARIA). ARIA can cause swelling or bleeding in the brain and may be asymptomatic. Radiologists must monitor for ARIA to plan image monitoring per established guidelines.
Researchers at the University of Sydney have developed a nanoscale optical technique to monitor protein aggregates forming in cells, which can lead to neurodegenerative diseases such as Alzheimer's and ALS. The study provides a new window into the transition of proteins from liquid to solid phase.
A new imaging technique, tau PET, has been shown to predict cognitive decline in Alzheimer's patients with greater accuracy than current methods. This breakthrough could lead to earlier diagnosis and treatment, improving patient outcomes.
The study reveals a double-layered structure of amyloid-β on GM1-containing membranes that acts as a catalyst for fibrillization. This discovery offers new insights into predicting Alzheimer's disease onset and potentially inhibiting its progression.
Scientists develop a method to construct crystalline artificial steric zippers in peptide β-sheets, paving the way for novel therapeutic strategies and materials. The research utilizes metal ions to prevent aggregation and form needle-shaped crystals with specific structural characteristics.
A new multi-center study found that having a genetic variant in the prealbumin gene alone is not sufficient for diagnosing transthyretin amyloid cardiomyopathy in older Black patients. Researchers suggest that a blood test measuring prealbumin levels may be useful in identifying patients at risk of developing cardiac amyloidosis.
Researchers found that Alzheimer's patients exhibit heightened sensitivity to light changes, which can contribute to 'sundowning' and disease progression. Light therapy could help manage these symptoms and potentially slow disease progression.
In a phase 3 clinical trial, donanemab significantly slowed clinical progression in patients with low/medium tau and high tau pathology. The treatment cleared brain amyloid plaque, demonstrating its potential to slow Alzheimer disease progression.
The latest Alzheimer's drug, donanemab, has shown encouraging results in slowing cognitive decline by 35% compared to placebo in patients with low-to-intermediate levels of tau. However, its effectiveness is limited for those with more advanced disease, and risks include serious side effects such as amyloid-related imaging abnormalities.
Researchers found that the amyloid precursor protein (APP) regulates human neurogenesis, which could be linked to Alzheimer's disease. APP promotes a balance between stem cell proliferation and differentiation, suggesting its disruption may cause premature neurogenesis and cellular stress.
Scientists at the Stowers Institute for Medical Research have uncovered the structure of the first step in amyloid formation for Huntington's disease. The team proposes a new method for treating not only Huntington's but potentially dozens of other amyloid-associated diseases by preventing the initial, rate-limiting step from occurring.
A groundbreaking study has shown that a devastating heart condition can spontaneously reverse in three men, who are now free of symptoms. The condition, transthyretin cardiac amyloidosis, is progressive and previously considered irreversible.
Defective myelin promotes disease-related changes in Alzheimer's by accelerating amyloid plaque deposition and overwhelming immune cells. Slowing down age-related myelin damage could lead to new therapies and prevent or slow down the disease.
A new study in a mouse model of Alzheimer's disease examines the effects of environmental enrichment on AD symptom progression and pathology. The researchers found that living in an enriched environment improved several measures of metabolism and reduced individual behaviors, which became more similar and rigid as the disease progressed.
Researchers found that a combination of amyloid burden and blood markers of abnormal astrocyte activation can predict Alzheimer's disease progression. Testing for these biomarkers may help identify patients at risk, enabling earlier diagnosis and treatment.
Researchers found that apoE4 poorly binds factor H, a regulatory factor of immunity, leading to amyloid-β oligomerization and neuroinflammation. This could be a potential solution to preventing Alzheimer's disease, with further research needed to find a bridging molecule.
Researchers have developed a pharmacological treatment that improves cardiac function in patients with stiff-heart syndrome, a condition caused by amyloid protein deposition. The new drug reduces amyloid protein deposits and shows promise in reversing established disease symptoms.
Researchers at Brigham and Women's Hospital have characterized the structure of amyloid-beta fibrils in the human brain, revealing their role in Alzheimer's disease progression. The study sheds light on how lecanemab, a US FDA-approved drug, exerts its protective effects by targeting these fibrils.
Researchers identified the structure of a special type of amyloid beta plaque protein associated with Alzheimer's disease progression. Lecanemab, an approved AD treatment, can bind and neutralize these small aggregates, potentially slowing cognitive decline in patients with early AD.
Research published in Radiology suggests that exposure to recurrent brain trauma, such as explosions, may increase the risk of developing Alzheimer's disease. Amyloid-beta protein accumulation was detected in six out of nine military instructors who were exposed to subconcussive blast injuries.
Researchers at Temple University Health System found that carbonic anhydrase inhibitors reduce inflammation, restore cell function and prevent cognitive impairment in mice with amyloid buildup. CAIs also improved cerebrovascular health and enhanced amyloid-clearing capacity.
Researchers have identified a possible way to help break the cycle between sleep disturbances and Alzheimer's disease. A small study found that people who took a sleeping aid experienced a drop in key Alzheimer's proteins.
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.