Articles tagged with Amyloids
A team of scientists found that the p75 receptor molecule has a neuroprotective effect on the sympathetic nervous system in mice with Alzheimer's disease, challenging the prevailing view of its harmful role. The study suggests that p75 could be a target for new protocols to manage dementia and memory loss.
Researchers created a computational model to examine the role of certain proteins in familial Alzheimer's disease. The model found no link between amyloid beta plaques and tau tangles, but suggested that genetic mutations in proteins and GSK3 over-activation may contribute to the development of the disease.
A team of researchers at the University of Michigan and the University of California, San Diego, have resolved a long-standing debate about how Alzheimer's disease kills brain cells. They found that amyloid-beta peptides form pores in brain cell membranes, allowing calcium ions to enter and trigger cell death.
Tiny, toxic protein particles severely disrupt neurotransmission and inhibit delivery of key proteins in Alzheimer's disease. The particles inhibit neurons from communicating with each other and with other target cells in the body.
Researchers have discovered a mode of action for mysterious protein snarls found in Alzheimer's patients, suggesting a combination therapy approach. The findings identify two proteins, amyloid beta and tau tangles, that wreak havoc on the nervous system, causing neural function loss and memory decline.
Researchers at Penn Medicine have developed a biomarker test that can confirm or rule out Alzheimer's disease by measuring cerebrospinal fluid concentrations of amyloid beta42 peptide and tau protein. The test accurately predicted the conversion from mild cognitive impairment to Alzheimer's disease in 81.8% of cases.
Researchers at Georgetown University Medical Center have found that a class of Alzheimer's disease drugs may prevent long-term damage from traumatic brain injury (TBI) in animals. The study suggests that gamma secretase inhibitors, designed to prevent build-up of amyloid peptide, could potentially do so.
Researchers identified a new amyloid beta mutation that hinders Alzheimer's disease progression by preventing the formation of amyloid fibrils. This discovery offers potential therapeutic strategies for both sporadic and genetic forms of the disease.
A study by Washington University School of Medicine found that individuals with lower levels of amyloid beta 42 in their cerebrospinal fluid had reduced whole brain volumes, suggesting early brain damage. The results suggest that Alzheimer's disease may harm the brain for years before symptoms appear.
Research reveals that amyloid plaques may increase astrocyte activity throughout the brain, affecting neuronal function and potentially offering new therapeutic targets. The study uses advanced imaging techniques to demonstrate synchronized calcium wave transmission across astrocytes in plaque-bearing mice.
Scientists have discovered a new therapeutic target for Alzheimer's disease by uncovering the normal function of a brain protein. The discovery suggests that the disease stems from an imbalance in signaling between neurons, rather than toxicity from amyloid plaques.
Researchers used lasers to visualize amyloid fibers in the lab and found that it can inhibit their growth and degrade them. This technique may offer a new approach to treat amyloid-based disorders like Alzheimer's, Parkinson's, and Huntington's diseases.
Researchers have discovered that two cardiovascular proteins, SRF and myocardin, work together in the brain's blood vessels to decrease blood flow and impair amyloid beta removal. Studies in human cells and mice show that these proteins increase toxic amyloid beta levels, contributing to Alzheimer's disease.
Scientists have found that a genetic risk factor for Alzheimer's disease slows down the brain's ability to export toxic amyloid-beta protein. The study suggests that when ApoE4 is present, the brain becomes less efficient at removing amyloid-beta, allowing it to accumulate and increase the risk of developing the disease.
Researchers investigate how neuronal activity leads to amyloid precursor protein (APP) cleavage and the formation of fibrous plaques in Alzheimer's disease patients. Treatment with a cdk5 inhibitor reduces APP association with BACE microdomains and cleavage.
A study found that recovery from brain injury increases amyloid beta levels in patients, with better neurological status correlating to higher levels. The findings suggest a new understanding of the connection between brain injury and Alzheimer's disease.
A virus that infects potatoes has been used to develop antibodies that can bind to the amyloid beta protein, a key contributor to Alzheimer's disease. Studies in mice have shown promising results, with the development of strong antibodies that can slow disease progression and improve cognitive function.
Researchers found that elevated calcium levels near amyloid plaques can disrupt neuronal function, leading to cellular degeneration. This study provides a new understanding of the connection between amyloid plaques and neurodegeneration in Alzheimer's disease.
Researchers found that PBT2 improves two indicators of executive function in Alzheimer's patients and reduces amyloid beta levels in the spinal fluid. The study suggests that PBT2 may be a promising treatment for improving cognitive performance in early-stage Alzheimer's disease.
Researchers at NYU Langone Medical Center presented several key findings on Alzheimer's disease risk factors, including a study that identified signs of brain pathology in healthy individuals. They also reported promising results from couples counseling and antibody tests against common mouth bacteria linked to Alzheimer's disease. The...
Researchers created a laboratory model to study Alzheimer's disease mechanisms at the molecular level. The model found that amyloid beta peptides cause a 'leaky' membrane, disrupting normal impulse transmission and leading to cell toxicity.
Researchers have discovered a new genetic risk factor, CALHM1, associated with late-onset Alzheimer's disease. The gene affects calcium levels and is linked to increased amyloid-ß peptides, forming brain plaques in the disease.
A study reveals a direct link between Alzheimer's disease-causing mutations and aberrant calcium signaling. The researchers found that this disrupted calcium release led to amyloid beta protein generation, a hallmark of the disease.
The study demonstrates that CNI-1493 protects nerve cells against amyloid beta-induced damage in culture and improves memory and cognitive function in mice prone to developing an Alzheimer's-like disease. The drug may provide a faster and more effective treatment for Alzheimer's, offering a promising alternative to current therapies.
Researchers analyzed DNA haplotype data from Iceland's genealogical database to identify the origin of hereditary cystatin C amyloid angiopathy (HCCAA). The study found that carriers lived a normal life span for 200 years before experiencing shortened lifespans, highlighting the impact of dietary changes on the disease.
Researchers identified a genetic variation associated with an earlier age of onset in Alzheimer's disease, which affects the brain's tau protein levels. The study suggests that these variations lead to higher tau levels in cerebrospinal fluid and earlier cognitive problems once amyloid plaques form.
Researchers found that interrupting a signaling pathway in immune system cells opened the possibility of a new strategy against Alzheimer's disease. Immune cells from outside the brain devoured plaque deposits, reducing their numbers by up to 90 percent.
Amyloid fibrils, bundles of ordered protein filaments, display remarkable mechanical properties and have potential as nanomaterials. They can be tailored and biocompatible, making them suitable for surfaces in medical technology and drug delivery systems.
A vaccine created by University of Rochester Medical Center scientists prevents the development of Alzheimer’s disease-like pathology in mice. The vaccinated mice demonstrated normal learning skills and functioning memory despite being genetically designed to develop an aggressive form of the disease.
Researchers from the University of Pennsylvania School of Medicine have discovered a small molecule that selectively targets and dismantles misfolded protein fibers connected to Alzheimer's disease and prion diseases. This breakthrough has implications for treating neurodegenerative diseases.
Researchers at the Salk Institute identified a probable molecular basis for the interaction between diabetes and Alzheimer's disease. The study found that damaged blood vessels in the brain of young diabetic mice suffered from significant memory loss and inflammation before any overt signs of Alzheimer's disease appeared.
Dr. Milan Fiala has received the 2008 Alzheimer Award for his work on phagocytosis of amyloid-beta and inflammation in Alzheimer's disease. His research suggests that the immune system's failure to clear waste products from the brain is a key contributor to the disease.
Researchers investigated the potential link between anesthetics and Alzheimer's disease. While desflurane alone did not increase amyloid-beta protein production, it stimulated cellular changes associated with Alzheimer's when combined with low oxygen levels.
A study has revealed that endocytosis is necessary for the production of amyloid beta, a key component of Alzheimer's brain plaques. The research found that endocytosis plays a critical role in increasing amyloid beta levels, which are coupled to normal nerve cell communication called synaptic activity.
Researchers used advanced imaging to examine brain tissue in mouse models of Alzheimer's disease, finding that amyloid plaques can develop in as little as a day and neuronal changes appear soon afterwards. The study provides new insights into the timing of brain changes associated with Alzheimer's dementia.
New research by University of Illinois at Chicago chemists identifies intermediate step in amyloid plaque formation as a toxic culprit. Tiny spheres averaging 20 nanometers assemble into sheet-like structures comparable to fibrils, making them more than 10 times poisonous.
Researchers have discovered a potential therapeutic approach to prevent the accumulation of toxic protein plaques in the brain, which are a hallmark of Alzheimer's disease. The study suggests that binding cystatin C to soluble amyloid beta prevents its aggregation into insoluble plaques.
A new study reveals that the intrinsic tendency of amyloid peptide Aß to aggregate determines its pathogenicity in Alzheimer disease. The researchers used a fruit fly model to identify the determinants of Aß's toxicity, finding a clear correlation between aggregation propensity and disease progression.
Biochemistry and biophysics expert Dr. James Shorter has been awarded a $1.5 million NIH New Innovator Award to develop biochemical methods for combating nerve degeneration diseases, including Parkinson's, Alzheimer's, and Huntington's.
Researchers discovered 'silent' seizures in mice with Alzheimer's disease, which may be related to cellular changes involving amyloid beta protein accumulations. These seizures could contribute to episodes of confusion in advanced Alzheimer's patients.
Recent mouse breeds designed to mimic Alzheimer's disease symptoms may not accurately reflect the human condition, according to a new study. The researchers suggest using alternative mouse breeds with only APP mutations to improve the accuracy of drug testing.
Researchers discovered that increasing the body's ability to absorb amyloid-beta in the blood leads to a decrease in brain levels, halting symptoms. A modified version of the sLRP protein showed promise in mice and humans, promising a new treatment option for Alzheimer's.
A team of researchers defined how metal ions bind to amyloid fibrils in the brain, appearing toxic to neurons. The findings suggest that only one way of binding appears toxic, while others may be harmless.
Researchers isolated bisdemethoxycurcumin, which boosts macrophages to clear amyloid beta plaques found in Alzheimer's disease. The study identified key genes involved in this process, offering a new treatment approach that targets the innate immune system.
Researchers have identified a protective role for normal prion proteins in preventing the formation of beta-amyloid plaques in the brain, a hallmark of Alzheimer's disease. High levels of PrPc reduced beta amyloid formation, while low or absent levels allowed it to return.
Researchers discovered a link between consuming foie gras and the formation of amyloid fibrils, which can accelerate AA amyloidosis in susceptible mice. The study suggests that people with a family history of diseases like Alzheimer's and rheumatoid arthritis may want to avoid consuming foie gras.
Researchers have discovered that stroke or traumatic brain injury can trigger Alzheimer's disease by enhancing the formation of brain-clogging amyloid plaques. Key findings include the role of caspase-mediated depletion of GGA3 in stabilizing BACE and increasing amyloid protein production.
Researchers at Massachusetts General Hospital have discovered a cellular chain of events linking stroke and head injury to Alzheimer's disease. The study reveals how brain cell death triggers the production of amyloid-beta protein, a key component of senile plaques.
Researchers identified a brain molecule, corticotropin-releasing factor (CRF), that increases amyloid beta levels in response to stress. Blocking CRF with a drug may provide a new way to decrease amyloid beta and delay or prevent Alzheimer's disease.
A study by Weill Cornell Medical College researchers found that immune antibodies penetrate neurons and reduce levels of Alzheimer's-linked amyloid peptides, offering new hope for immunotherapy against the disease. The discovery could also advance treatment for other immune diseases.
Researchers have discovered that Alzheimer's, Parkinson's, and type 2 diabetes share a common molecular mechanism, involving amyloid fibrils with a universal 'molecular zipper' structure. This finding could lead to new diagnostic tools and treatment options through 'structure-based drug design'.
A study by UC Irvine scientists found that diets rich in docosahexaenoic acid (DHA) can help prevent the development of Alzheimer's disease later in life. Mice given a DHA-rich diet showed lower levels of tau and beta amyloid, proteins associated with neurofibrillary tangles and plaques.
A study by Massachusetts General Hospital researchers found that blocking immune cell action increased amyloid-beta deposits and shortened life spans in a mouse model of Alzheimer's disease. The study suggests potential new therapeutic strategies for early-stage Alzheimer's disease.
A team led by Massachusetts General Hospital confirms that Pittsburgh Compound B binds to amyloid-beta protein in the human brain, a key step in Alzheimer's disease diagnosis. The findings support using PET imaging with PiB to track treatment results and emphasize the need for clinical symptom evaluation.
Researchers at the University of Pennsylvania found that common inhaled anesthetics increase amyloid plaque appearance and cognitive decline in genetically engineered mice. The study suggests a potential link between long-term anesthesia use and early-onset Alzheimer's disease.
A Scripps research study reveals the dynamic structural details of single prion molecules, shedding light on normal folding mechanisms and abnormal amyloid fibril conversion. The findings may lead to novel therapeutic targets for neurodegenerative diseases.
Researchers have identified a new genetic clue that may contribute to the development of late-onset Alzheimer's disease. Variations in the SORL1 gene were found to be associated with an increased risk of the disease, and altering the levels of this protein changed the way amyloid beta fragments were produced in cells.
Researchers identified a new genetic risk factor associated with late-onset Alzheimer's, implicating the SORL1 gene. Variants of this gene are linked to an increased risk of Alzheimer's, particularly in Caucasians, and may play a role in the production of toxic amyloid-beta fragments.
Researchers at the University of Toronto have identified a new gene, SORL1, associated with an increased risk of Alzheimer's disease in different ethnic groups. The discovery highlights the complexity of the disease's genetics and underscores the need for further replication studies.
Researchers discovered a genetic variation that enables adults to express higher levels of fetal hemoglobin, reducing their risk of Alzheimer's disease. The study also found that beta amyloid peptide has an affinity for adult hemoglobin, which may enhance its ability to wreak havoc in the brain.