Articles tagged with Amyloids
A research team at Kumamoto University identified a plant-derived molecule, PGG, that breaks down transthyretin (TTR) amyloid linked to heart and nerve disorders. The study found PGG effectively disassembled amyloid fibrils without disrupting other types of protein aggregates.
Researchers found that noninvasive measures of brain blood flow and oxygenation are associated with hallmark brain changes in older adults with and without cognitive impairment. Higher values on these indicators were linked to lower levels of amyloid plaques and larger hippocampal volume, indicating a lower risk of Alzheimer's disease.
The AMALIA project develops a scalable screening platform to identify anti-amyloid therapies, bypassing the challenge of studying amyloid nucleation. This approach enables parallel discovery campaigns on multiple targets, offering unprecedented speed and scalability.
A new study from the Stowers Institute has identified a mechanism that makes fleeting moments unforgettable, revealing a critical step in forming long-lasting memories. The research discovered a specific type of chaperone protein that allows proteins to change shape and form functional amyloids that house long-term memory.
Researchers developed a new tool, FibrilPaint combined with the FibrilRuler test, to measure the length of toxic Tau amyloid fibrils directly in solution. This 'molecular ruler' represents a major advance in understanding how these fibrils grow, break, and respond to potential drugs.
Researchers at UC Irvine found that amyloid precursor proteins form a complex with voltage-gated proton channels in human brain immune cells, altering their operation and promoting neuroinflammation. The study suggests two specific mutations linked to early-onset Alzheimer's further increase channel activity.
Protein clumps associated with Parkinson's disease can actively break down ATP, draining brain cells of vital energy. Researchers discovered that these clumps transform into molecular machines when they bind to ATP, highlighting a new mechanism of damage.
Researchers developed a nanotechnology strategy that reverses Alzheimer's disease by targeting the blood-brain barrier and restoring its natural waste-clearing pathway. The therapy achieved a significant reduction in amyloid-β levels and improved cognitive function in mouse models, showing promise for treating dementia.
A new study found that adipose-derived extracellular vesicles, tiny cell messengers in obese individuals, accelerate the buildup of amyloid-β plaques in the brain, a hallmark of Alzheimer's disease. Researchers hope targeting these tiny cell messengers could reduce the risk of Alzheimer's disease in people with obesity.
A study by researchers at the University of São Paulo identified high levels of neuroinflammation in young individuals with Down syndrome, contributing to the high prevalence of Alzheimer's disease. The discovery paves the way for disease prevention strategies and personalized treatments.
A study found that older adults with Parkinson's disease have a higher rate of brain amyloid positivity compared to younger patients, even without dementia. The researchers suggest this may indicate an accelerated transition from healthy cognition to dementia in PD patients.
Researchers found that individuals from African American, Hispanic and Asian groups were less likely to have elevated amyloid in the brain based on blood levels of p-tau217. This finding suggests that these groups may have a lower prevalence of amyloid and are not at sufficient risk to qualify for amyloid-lowering trials.
The Fork It Fund has awarded $1 million to support a major initiative at Stevens INI, accelerating scientific discovery by making critical research data more accessible worldwide. GAAIN is a global data-sharing platform connecting Alzheimer's disease and dementia-related data repositories from around the world.
Researchers at St. Jude Children's Research Hospital found that midkine protein prevents Alzheimer's disease by blocking amyloid beta assembly growth. Midkine inhibits amyloid beta elongation and secondary nucleation, two specific phases during assembly formation.
UCSF scientists identified a receptor that enables microglia to engulf and digest amyloid beta plaques, leading to fewer and smaller clumps. This discovery creates an opportunity for new therapies targeting the receptor ADGRG1.
A Johns Hopkins study identifies over 200 types of misfolded proteins associated with age-related cognitive decline in rats. The findings suggest that these proteins may contribute to Alzheimer's and dementia beyond just the previously known A-beta and tau amyloids.
A new brain imaging benchmark may improve how researchers classify biologically meaningful changes associated with Alzheimer’s disease. Researchers found a tau cut-point that distinguished individuals with cognitive impairment from those aging normally, but its effectiveness was limited in non-Hispanic Black participants.
Pernilla Wittung-Stafshede joins Rice University's Department of Chemistry as a professor, bringing expertise in metalloproteins and protein aggregation to enhance cancer research. Her focus is on understanding the role of copper-binding proteins in cancer metastasis and potential future therapies.
Research found that approximately 50% of participants with late-life depression and bipolar disorder showed tau accumulation in their brains, compared to only about 15% of healthy controls. The study suggests that neurodegenerative diseases, including Alzheimer's, can initially manifest as psychiatric symptoms.
A study published in Alzheimer's & Dementia found that learning one's Alzheimer's risk can decrease negative emotions like depression and anxiety, but also leads to decreased motivation for maintaining healthy lifestyle changes. Researchers emphasize the importance of personalized disclosure processes to sustain healthy behaviors.
Researchers identified CLU protein as a potential strategy to protect against Alzheimer's disease by increasing clusterin protein. Increased CLU protects the brain from amyloid plaques and loss of synapses, while identifying individuals most likely to respond based on their genetics.
Researchers trained AI to predict protein clumping linked to 50 human diseases. The new tool, CANYA, revealed specific chemical patterns driving or preventing harmful protein folding.
Calmming the brain's immune cells via norepinephrine may prevent or lessen Alzheimer's inflammation and damage. The study highlights a key role of norepinephrine in mitigating early inflammatory changes and neuronal injury.
A novel AI tool, RibbonFold, predicts the structures of amyloids, revealing previously overlooked nuances in their formation and evolution. This breakthrough may reshape how researchers approach neurodegenerative disease treatment and offers a scalable method for analyzing harmful protein aggregates.
Researchers found that SIRT2, a previously unknown enzyme, plays a key role in excessive GABA production associated with Alzheimer's disease. This process leads to brain inflammation and memory impairment. By targeting SIRT2, scientists can selectively block its harmful effects on memory without affecting other brain functions.
Researchers have initiated a clinical trial using an investigational medicine to lower amyloid precursor protein, targeting Alzheimer's disease in adults with Down syndrome. The study aims to prevent the development of Alzheimer's disease by addressing its underlying genetic cause.
A new study by UCL researchers found that people with visual Alzheimer's disease have a unique distribution of proteins and markers in their brain, leading to symptoms such as reading difficulties. In contrast, those with memory-led Alzheimer's disease have different protein patterns, resulting in symptoms like memory loss.
Angel Martí, a leading researcher on chemistry and nanostructures, has been awarded the Robert Holland Jr. Award for his groundbreaking work. He is recognized for his contributions to advancing scientific discovery and fostering talent in STEM fields.
A new Northwestern University study found that enhancing the brain's immune cells can clear Alzheimer's plaques and restore a healthier brain environment in immunized patient brains. The findings could reshape the future of Alzheimer's treatments by shifting the focus from removing plaques to harnessing the brain's natural defenses.
A study by Washington University in St. Louis researchers has found a critical role for the physical interfaces of amyloid beta peptides in determining their chemical dynamics, leading to neurodegeneration. The research identified small molecules capable of breaking the toxic feedback loop, providing evidence that proper nutrition may ...
Researchers from Osaka University found that peristaltic pump action promotes amyloid nucleation in supersaturated fluids, including blood and cerebrospinal fluid. High shear stress caused by the pumping motion mechanically breaks supersaturation to induce amyloid formation.
Researchers at the University of Florida have discovered a novel genetic mutation associated with an accumulation of toxic proteins in Alzheimer's brains. The study found that people carrying a specific variation of this repeated DNA strand have more than double the risk of developing late-onset Alzheimer's.
A study at Lund University found that brain trauma triggers Alzheimer's disease through vascular changes, challenging existing paradigms. The research team identified increased aggregation of amyloid-beta and vascular alterations in patients with traumatic brain injury.
Researchers from the University of Gothenburg have made a breakthrough in understanding the role of protein tau in Alzheimer's disease. By identifying specific amino acid modifications that occur before thread-like fibrils form, scientists hope to develop complementary drugs to combat the disease.
Researchers discovered that pancreatic β cells produce a neuroprotective agent called Fibroblast Growth Factor 23 (FGF23), which can stop amyloid-β-induced neuronal cell death. FGF23 may increase ribosomal proteins, helping to maintain homeostasis in neurons.
A study found that people with delayed REM sleep have higher levels of toxic proteins amyloid and tau, and lower levels of healthy protein BDNF, which can increase the risk of developing Alzheimer's. Practicing healthy sleep habits may help mitigate this risk.
Researchers found that individuals with childhood epilepsy have an increased accumulation of brain amyloid later in life, which may lead to late-onset brain amyloid disorders like Alzheimer's disease. The study also showed that these individuals performed worse in cognitive tests compared to controls.
A new study suggests that stalled amyloid protein production contributes to the development of Alzheimer's disease. Researchers found that rare familial genetic mutations linked to early-onset dementia cause deficiencies in multiple APP processing steps, leading to neurodegeneration.
Regular aerobic exercise has been shown to significantly reduce disease markers associated with Alzheimer's, protecting healthy brain cells and restoring balance in the aging brain. The study highlights the potential for aerobic exercise to serve as a cornerstone in preventive strategies for Alzheimer's.
Dr. Gail Cornwall is investigating the structure of the brain extracellular matrix, a network of proteins and polysaccharides found in the space between neurons and glia. Her research aims to identify novel structural elements and mechanisms that enable brain plasticity and sex-specific responses.
Researchers investigate how perturbed gene expression contributes to neurodegenerative disorders like Alzheimer's. Alternative polyadenylation, a mechanism regulating protein production, is being studied for its potential role in the disease.
Researchers at Washington University in St. Louis are developing vaccines to target misfolded proteins in the brain, with a focus on preventing inflammation and using peptide nanofibers. The goal is to prevent dementia by training the immune system against amyloid beta and tau proteins.
Researchers at the Buck Institute found that ketone bodies interact directly with misfolded proteins, altering their solubility and structure to be cleared through autophagy. This discovery suggests a new form of metabolic regulation of protein quality control in the brain, with potential therapeutic applications.
Researchers evaluated over 400 patients with suspected Alzheimer's disease and found that CSF analysis was less reliable than PET imaging. The study suggests using amyloid PET scans as the diagnostic method of choice, especially for those with gray area results between 5.5-7.1 in their CSF.
Researchers at UCL found that excess brain volume loss with amyloid-targeting immunotherapies is associated with therapy effectiveness, not harm. The 'amyloid-removal-related pseudo-atrophy' or ARPA phenomenon suggests that removal of amyloid plaques may be the cause of observed brain changes.
Alzheimer's researchers identify specific inhibitors that prevent nerve cell loss and improve social recognition memory in mouse models. The study sheds light on the molecular sequence of events leading to cellular demise and opens up new research avenues for halting or preventing brain damage.
A team of researchers at the University of Toronto has developed a rapid screening system to identify compounds that can stop the growth of amyloid proteins. The study found 40 compounds that demonstrate the ability to inhibit amyloid formation, providing a promising lead for future disease treatments.
Researchers have uncovered a new mechanism in the growth of amyloid β (Aβ) fibrils, which are closely associated with Alzheimer's disease. The team found that each Aβ fibril is composed of two thin strands called protofilaments, and when their ends align, the fibril enters a paused state where growth temporarily stops.
Researchers validate a new blood test platform that can measure multiple biomarkers of Alzheimer's disease, potentially improving early diagnostics and treatment. The platform captures changes in proteins related to neurodegenerative diseases and may help track disease progression over time.
Researchers have uncovered a critical mechanism by which mutant p53 protein converts other proteins into cancer-promoting agents, driving tumor growth. Heparin, a widely used anticoagulant, can inhibit the formation of these harmful aggregates, providing a potential therapeutic approach.
A study published in the journal Brain shows that increases in protein levels with new Alzheimer's drugs can explain the slowing of cognitive impairment at least as well as the reduction in amyloid plaques. The researchers found that higher levels of a critical brain protein correlate equally well with cognitive benefits.
Researchers investigated the connection between androgen deprivation therapy for prostate cancer and Alzheimer's disease. They found that ADT can exacerbate cognitive decline by increasing brain immune cell infiltration, but a combination with Natalizumab improved integrity of the blood-brain barrier and reduced inflammation.
A new study found that one in 1,000 people in the UK carry genetic variants linked to cardiac amyloidosis, a potentially fatal heart condition. The study also revealed higher incidence rates among individuals with African ancestry, highlighting the need for early detection and monitoring.
A new study from Washington University School of Medicine found that people with multiple sclerosis are less likely to develop the molecular hallmarks of Alzheimer's disease. The discovery suggests a potential new avenue for treating Alzheimer's and could inform therapeutic strategies.
Researchers question the effectiveness of new amyloid immunotherapy drugs in reducing Alzheimer's disease impact, citing limited eligibility and high costs. The drugs showed small effect sizes that may not outweigh the risk of adverse events.
Researchers found high diagnostic accuracy for identifying Alzheimer's disease using amyloid probability score 2 blood test and p-tau217 levels. The study suggests blood tests could influence clinical care, warranting further evaluation.
The A4 study, a large clinical trial of pre-symptomatic Alzheimer’s disease, has yielded key insights into the condition. Researchers have collected extensive data on brain scans, blood samples, genetic information and cognitive tests from over 7,500 participants.
Oligodendrocyte-derived amyloid beta produces toxic peptide that promotes neuronal dysfunction in Alzheimer's disease. Selective suppression of oligodendrocyte Aβ production rescues abnormal neuronal hyperactivity, suggesting targeting these cells as a promising therapeutic strategy for AD.
Researchers at Wash U used single-molecule orientation-localization microscopy to study the nano-architecture of amyloid fibrils, revealing their growth and decay patterns. They found multiple ways A-beta can remain stable or grow and decay, with surprising results on its underlying structure.
Researchers have developed a multi-component hydrogel scaffold to mimic the amyloid-beta containing microenvironment associated with AD. The study found elevated levels of neuroinflammation and apoptosis markers in healthy neuronal progenitor cells cultured within this environment.