Articles tagged with Amyloid Hypothesis
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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 at the University of Bath develop a peptide fragment that locks alpha-synuclein into its healthy shape, blocking toxic clumps that cause nerve cell death. The breakthrough demonstrates the potential of rational peptide design to transform large proteins into compact drug-like molecules.
Researchers developed a blood test that accurately diagnoses Alzheimer's disease and measures its progression. The test correlates with the amount of tau aggregates in the brain, distinguishing between early- and late-stage diseases.
A clinical trial shows that removing amyloid plaques from the brain can delay Alzheimer's symptoms, supporting the amyloid hypothesis. The treatment reduced the risk of developing dementia in people destined to develop early-onset Alzheimer's disease.
A review article reveals CD2AP's crucial role in amyloid metabolism, tau pathology, synaptic function, and neuroinflammation in Alzheimer's disease. CD2AP deficiency accelerates plaque formation, while its loss in neurons leads to reduced spine density and impaired synaptic plasticity.
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.
University Hospitals Brain Health & Memory Center is now treating patients with KISUNLA, a medication approved by the FDA to treat Alzheimer's disease. The treatment has shown promise in clinical trials and may be an option for patients with mild cognitive impairment and mild dementia.
Scientists have successfully imaged superspreader fibrils in the brain tissue of Alzheimer's patients, shedding light on their role in spreading the disease. The study, published in Science Advances, uses advanced imaging techniques to visualize the fibrils' formation and spread.
Researchers have developed a peptide inhibitor called RI-AG03 that effectively prevents Tau protein aggregation in lab and fruit fly studies. The breakthrough targets both major aggregation-promoting 'hotspots' of the Tau protein, potentially paving the way for more effective treatments for neurodegenerative diseases.
A new study found that amyloid-beta and tau proteins affect brain activity differently, with increased levels leading to hyperactivity and decreased levels resulting in hypoactivity. Participants with higher rates of this brain slowing showed greater cognitive decline in attention and memory.
A $3.9 million grant from the National Institutes of Health supports a study on wearable sleep trackers and AI in predicting blood biomarkers of Alzheimer's disease in at-risk individuals. The research aims to create an 'early warning system' for flagging individuals with a genetic predisposition to Alzheimer's.
Researchers discovered that amyloid fibrils can harness quantum superradiant effects to mitigate oxidative stress, potentially transforming dementia treatments and understanding of Alzheimer's disease. This finding raises questions about the conventional view of amyloid's role in the disease.
A team led by Emory researchers found strong evidence supporting a new understanding of the mechanism behind Alzheimer's disease. They identified more than 20 proteins that co-accumulate with amyloid beta, suggesting they may play an important role in brain damage rather than the amyloid itself.
Researchers found that dopamine treatment increased neprilysin levels and reduced beta-amyloid plaques in mouse brains, improving memory function. Long-term L-DOPA treatment also showed improved cognitive performance in mice.
Researchers investigated the relationship between protein aggregation and liquid-liquid phase separation, finding that droplet formation may actually protect against aggregation. The study, led by Paul Scherrer Institute, used over 500 conditions to test the behavior of alpha-synuclein proteins.
Researchers found that baseline amyloid burden and brain health are stronger predictors of Alzheimer's progression than age alone. The study also showed that individuals with higher amyloid levels developed dementia two years earlier than those without.
Zarbio and Georgia State University scientists propose a framework for understanding Alzheimer's disease, linking molecular mechanisms, beta-amyloid biomarkers, and diagnosis. The Amyloid Degradation Toxicity Hypothesis resolves long-standing paradoxes in AD research.
Researchers found that a rare genetic mutation in the APOE gene, known as the Christchurch mutation, may prevent Alzheimer's dementia by severing the link between amyloid and tau accumulation. This discovery offers new hope for preventing the disease.
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.
Scientists at the University of Rochester Medical Center discovered a link between Alzheimer's disease and hearing loss in mice, finding that plaque location in the brain may contribute to hearing decline. The study suggests that tracking disease progression through amyloid PET imaging could be a potential biomarker for hearing loss.
New research from UC Berkeley suggests that deep sleep can act as a protective factor against memory decline in individuals with existing high amounts of Alzheimer's disease pathology. This study provides hope for alleviating some of dementia's most devastating outcomes.
Researchers examined associations between APOE ε2 and ε4 alleles, polygenic profiles, and Alzheimer's disease biomarkers. They found links between ε4 alleles with plasma and CSF Aβ42 and CSF tau, as well as differences in associations with tau and Aβ42.
A recent study from the University of Eastern Finland suggests that previous traumatic brain injury may increase the risk of frontotemporal dementia (FTD), particularly in individuals without a genetic mutation. Patients who suffered head injuries developed FTD earlier than others, on average.
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.
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 have identified a new gene, NUCL-1, in the transparent roundworm C. elegans, which is linked to human neurodegenerative diseases such as ALS and Alzheimer's. The discovery challenges recent theories on the role of nuclear structures in these disorders.
Neurobiologists identified mechanisms underlying atypical protein tangles that kill neurons in neurodegenerative disorders. Engineering Drosophila adults with human Tau revealed a 'traffic jam' effect, where reduced retromer activity accelerates neurodegeneration. Inhibiting the shortened form of Tau could stall neuron loss.
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.
Researchers developed a new method to screen drugs for treating Alzheimer's disease, shedding light on why current treatments have been ineffective. The study identified new targets for drug development by analyzing disease mechanisms in human neurons.
A new clinical trial is enrolling young people with rare genetic mutations that cause early-onset Alzheimer's disease. The study will test gantenerumab to prevent the buildup of toxic protein amyloid beta, which can slow or stop the disease.
The study, published in Nature Aging, found that sildenafil reduces the likelihood of developing Alzheimer's disease by 69% compared to non-users. Sildenafil also shows promise in treating the disease by increasing brain cell growth and decreasing hyperphosphorylation of tau proteins.
Researchers at ETH Zurich have made a groundbreaking discovery that protein amyloids can self-replicate, challenging the long-held RNA hypothesis as the origin of life. The findings suggest that early life forms may have used amyloids as information carriers and catalytic units.