Articles tagged with Amyloidosis
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Researchers at NYU Langone Health have identified a new target for preventing Alzheimer's disease, targeting the mechanism behind neural and vascular death. The study suggests that Carbonic Anhydrase Inhibitors may be effective in delaying symptom onset and improving quality of life for patients.
Researchers have unveiled a new diagnostic tool that can identify Alzheimer's disease long before the onset of symptoms using a non-invasive eye scan. The tool, developed by Professor Melanie Campbell, uses polarized light to highlight amyloid protein deposits in the retina.
Researchers at TSRI have identified 79 potential molecules that activate the ATF6 arm of the UPR, a signaling network that enhances editing or protein quality control. The compounds mimic the normal activation of ATF6, leading to the generation of chaperone proteins that can help prevent misfolding events associated with disease.
A recent study found that estrogen therapy via skin patch reduced beta-amyloid deposits in the brains of newly postmenopausal women, potentially decreasing Alzheimer's disease risk. Women with a greater genetic risk for Alzheimer's, such as those with the APOE e4 genotype, particularly benefited from this therapy.
Researchers found that treatment with an anti-platelet drug reduces amyloid plaques in cerebral vessels, improving brain perfusion. Alzheimer's disease is characterized by the formation of protein agglutination and deposits of amyloid in the brain, leading to progressive cognitive decline.
A new study finds that human amyloid-beta is protective against infections in mice and roundworms, and may lead to new treatments for Alzheimer's disease. The protein's oligomeric form appears to entrap microbes, providing a natural defense mechanism.
Researchers at the University of Bergen have found a link between a gene defect and Alzheimer's disease, identifying protein PITRM1 as a crucial factor in disease development. The study suggests that reduced levels of this protein may lead to increased amyloid deposition in the brain.
A team of scientists at Linköping University has developed a molecular probe for early detection of amyloidosis, a rare disease affecting less than 200,000 people in the US. The probe detects small amyloid deposits that traditional methods miss, enabling earlier diagnosis and more effective treatment.
Researchers have identified a powerful drug, SOM0226 (tolcapone), that can significantly improve the pharmacological treatment of familial transthyretin amyloidosis (ATTR). Tolcapone has been shown to inhibit the aggregation of amyloid fibers by TTR and stabilize the protein structure, slowing down disease progression.
Researchers found that magnesium-L-threonate alleviated cognitive decline in mouse models of Alzheimer's disease by suppressing Aβ deposition. The study suggests that magnesium ions target APH-1α/1β, inhibiting the aggregation of β-amyloid protein and resulting in improved cognitive function.
Scientists have unraveled the abilities of multinucleated giant cells, which help the body deal with bulky items that obstruct physiological processes. The treatment for systemic amyloidosis has been found to be effective due to the complement system's role in marking and destroying protein deposits.
A team of researchers discovered a molecular mechanism responsible for familial amyloidosis and other life-threatening diseases, including Alzheimer's and Parkinson's. They found that specific mutations can alter the protein's structure, leading to abnormal clumping and organ damage.
Patients with light-chain (AL) amyloidosis treated with high-dose chemotherapy and autologous stem cell transplantation have the greatest success for long-term survival. Nearly one-third of patients achieved up to 20-year survival after treatment.
A new study found a variant in the IL1RAP gene associated with higher rates of amyloid plaque accumulation and cognitive decline in Alzheimer's patients. The research suggests targeting the IL1RAP immune pathway may be a viable approach for clearing amyloid deposits and fighting disease progression.
A Phase 3 clinical trial has been launched to evaluate the efficacy and safety of a novel RNAi investigational agent for treating patients with transthyretin-mediated familial amyloidotic cardiomyopathy (FAC). The first US patient, Leon Silas, 76, was enrolled in the study after being diagnosed with congestive heart failure in 2011.
A new molecular imaging scan detects dangerous protein deposits in the heart, significantly increasing cardiac risk. The scan uses a widely available agent to assess amyloid buildup and predict future heart attacks.
A study found that repetitive head injuries can lead to the build-up of beta-amyloid in the brain, increasing the risk of dementia. Boxers were most affected, with four times more likelihood of developing beta-amyloid deposits and worse disease outcomes.
Research found that brain amyloid stimulates pancreas fibril growth and vice versa, raising hopes for understanding the connection between AD and T2D. Islet amyloid peptide, derived from pancreatic cells, is also present in human brain senile plaques.
Research participants who reported greater sleepiness had higher amyloid accumulation in cerebral cortex regions heavily affected in Alzheimer's disease. This suggests that sleep disturbance may be an early target for intervention to prevent cognitive deficits.
Researchers found that Golgi fragmentation accelerates APP trafficking and production of toxic Aβ protein in AD. Rescuing the Golgi by blocking cdk5 or GRASP65 reduces Aβ accumulation, offering a potential therapeutic strategy for slowing Alzheimer's progression.
Investigators from Massachusetts General Hospital developed a novel culture system that reproduces the full course of events underlying Alzheimer's disease. The system confirms the amyloid hypothesis, which suggests that deposition of beta-amyloid plaques in the brain is the first step in a cascade leading to neurodegenerative disease.
Researchers at Gladstone Institutes found that progranulin deficiency can increase amyloid-beta plaque formation, neuroinflammation, and cognitive dysfunction in a mouse model of Alzheimer's disease. Increasing progranulin levels via gene therapy effectively prevented these abnormalities and protected against cell death.
The Houshiheisan compound prescription effectively suppresses abnormal amyloid precursor protein accumulation and reduces amyloid substance deposition. It maintains the stabilization of the internal environment of neurovascular units, minimizing injury to these units in the ischemic penumbra.
Research from UC Davis Health found that high HDL and low LDL cholesterol levels are associated with lower brain amyloid plaque deposits, a hallmark of Alzheimer's disease. This study provides evidence for the importance of cholesterol management in preventing cognitive decline.
A recent study led by Boston University School of Medicine researchers found that diflunisal successfully reduced neurological decline and preserved quality of life in patients with familial transthyretin amyloidosis. This repurposed generic drug demonstrates an effective alternative to liver transplantation for this devastating disease.
A study found increased deposits of β-Amyloid (Aβ) plaques in some areas of the brains of patients with traumatic brain injury (TBI). Researchers discovered Aβ plaque increases may be linked to TBI and accelerated Alzheimer's Disease progression.
Researchers have generated disease-specific induced pluripotent stem cell lines from a patient with familial transthyretin amyloidosis (ATTR), a lethal protein-folding disorder. The study successfully recreates essential aspects of the disease in vitro, validating this iPSC-based system as a platform for testing therapeutic strategies.
Researchers identify amylin protein deposits in Alzheimer's disease brains, linking it to age-related dementia and Alzheimer's. Amylin accumulation may be therapeutic target for drug development.
Researchers found that cognitively normal people with high amyloid levels are likelier to develop dementia. Mayo Clinic neurologists also developed a test to gauge concussion severity using autonomic reflex testing, and discovered heart attack victims who received therapeutic hypothermia are unlikely to suffer cognitive impairment.
A recent genome-wide imaging study has discovered a new gene, BCHE, associated with Alzheimer's plaques. The study found that variants of the BCHE gene are significantly linked to increased levels of amyloid plaque deposits in the brains of patients and those at risk for the disease.
Researchers found that white matter hyperintensities (WMHs) are equally associated with an Alzheimer's diagnosis as amyloid plaque. WMHs were also predictive of which subjects with mild cognitive impairment would go on to develop Alzheimer's. The study suggests potential ways to prevent Alzheimer's in those with amyloid deposits.
A new PET test using 11C-PIB offers a non-invasive method to visualize amyloid deposits in the heart, providing valuable information for disease prognosis and treatment monitoring. The study demonstrated positive uptake of 11C-PIB in patients with cardiac amyloidosis.
Researchers developed a plaque-specific antibody that clears existing β-amyloid deposits in Alzheimer's disease mice, promoting potential treatment development. The study suggests that targeting insoluble amyloid beta is critical for plaque removal without microhemorrhage side effects.
A study published in Alzheimer Disease & Associated Disorders found that a florbetapir PET scan can alter physicians' diagnostic thinking, guiding treatment and further testing for patients with cognitive impairment. The test showed amyloid deposits in 113 out of 229 patients, leading to changes in diagnosis and treatment plans.
Researchers at LSU Health Sciences Center have identified Monoacylglycerol lipase (MAGL) as a promising therapeutic target for treating or preventing Alzheimer's disease. Inactivation of MAGL reduced beta amyloid plaque production and improved brain function, learning, and memory.
Neutrophil extracellular traps (NETs) release DNA-made traps that break down amyloid fibrils into smaller toxic pieces. This process is linked to the aggravation of amyloidosis, a group of clinical syndromes characterized by deposits of amyloid fibrils throughout the body.
A multicenter observational study found that Black patients with the V122I mutation have a median survival time of 26 months after diagnosis, with declining heart function and quality of life. The study establishes an increased risk of death from cardiac amyloidosis among carriers of this mutation, particularly after age 60.
Researchers found that the CyBorD/CVD regimen can lead to complete hematologic response and may make AL amyloidosis patients eligible for stem cell transplants. This effective multiple myeloma treatment is already widely used, offering a potential therapy for those with few treatment options.
Researchers have discovered that myocilin deposits can lead to vision loss in glaucoma patients. The study, published in the Journal of Molecular Biology, explores one of the molecular origins of glaucoma and potentially leads to new treatments.
Researchers found that vitamin D reduces inflammation and debris buildup in mouse eyes, improving vision. Vitamin D also triggers macrophages to change configuration, reducing damage and promoting clear vision. The study suggests a potential simple way to prevent age-related macular degeneration.
Treatment with high-dose melphalan and autologous stem cell transplantation achieved a high organ response rate and increased overall survival, even in patients without hematologic complete response. The study found that careful patient selection and experienced management can lead to low treatment-related mortality rates.
A study using advanced brain imaging techniques found that 33% of participants had high levels of amyloid-beta deposits, indicating an increased risk of Alzheimer's disease. The study also discovered a link between these deposits and changes in brain metabolites, which may help identify people at risk for the condition.
A study found that individuals with amyloid plaques and no cognitive impairment exhibited similar brain structure changes to those with Alzheimer's disease. The researchers aim to identify potential therapeutic targets to prevent the development of dementia.
A study using functional MRI scans found that individuals with the APOE4 gene variant exhibit abnormal brain function before forming senile plaques characteristic of Alzheimer's. Researchers aim to identify high-risk patients and develop treatments to slow disease progression.
Researchers at the Hertie Institute of Clinical Brain Research have found that peripheral administration of misfolded protein fragments can induce Alzheimer's-like brain pathology in mice. This discovery provides new clues on the underlying mechanisms of Alzheimer's disease and may lead to new strategies for prevention and treatment.
Researchers found that people with APOE ε4/ε4 gene type have differently shaped brain protein deposits compared to those with the neutral risk gene type. The findings suggest that different shapes might respond differently to treatments, supporting a hypothesis that APOE genotype changes amyloid structure.
Researchers discovered a specific mutation that promotes fibril development, leading to organ damage and death. The study suggests this finding could be a target for future drug development in treating the fatal condition.
Researchers discovered that regions of the brain with increased amyloid-beta deposits are not the same as those with atrophy due to neuron loss. The study found that these regions can disrupt connections with the hippocampus, leading to neuron death.
Researchers found a greater number of protein clumps linked to Alzheimer's, especially among children of mothers with the disease. The study suggests a genetic mechanism is involved and may help explain why family history is a significant risk factor for the brain disease.
A new investigational drug, bapineuzumab, has been shown to reduce amyloid-β deposits in the brain by 25% in patients with mild-to-moderate Alzheimer's disease. This breakthrough finding could help assess the efficacy of other drugs for Alzheimer's treatment.
A new instrument called PIB-PET effectively detects amyloid-beta protein plaques in the brains of living people, predictive of who will develop Alzheimer's disease. The study confirms the sensitivity of the tool and provides strong evidence supporting the 'amyloid hypothesis'.
Researchers use Positron Emission Tomography (PET) to image amyloid-beta protein plaques in the brain, detecting deposits in cognitively normal older subjects and associating them with brain atrophy. The findings suggest a critical early role for amyloid deposition in Alzheimer's disease development.
Scientists at the University of Leeds have discovered that amyloid fibres are toxic and become more damaging when shorter, challenging accepted thinking about their inert nature. The study highlights a potential new area for therapeutics and may lead to the development of new treatments for diseases such as Alzheimer's and Parkinson's.
The Arlene and Arnold Goldstein Family Foundation has donated $1.5 million to support research at Scripps Research Institute, aiming to develop new drugs for transthyretin amyloidosis. This collaboration will also explore senile systemic amyloidosis, a type of the disease affecting a quarter of the population 85 years old or older.
Researchers at UCL have identified a protein, SAP, as a potential therapeutic target for Alzheimer's disease. CPHPC, a new small molecule drug, removes SAP from the blood and brains of patients with Alzheimer's disease, showing promising results.
Researchers developed a test to quickly assess the effectiveness of Alzheimer's drugs in reducing amyloid beta production, which builds brain plaques. The test, SILK, was used to study LY450139, an Eli Lilly drug candidate, and showed a dose-dependent drop in A-beta production.
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.
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.
The study finds that Pittsburgh Compound B can detect amyloid deposition in the brains of clinically older adults, potentially opening the door to early diagnosis and prevention strategies. Detailed tests show no decrease in functioning among participants with Alzheimer-associated plaques, suggesting a window of opportunity to slow or ...
Researchers reduce Aβ42 deposits by overexpressing NEP enzyme in fruit flies, suppressing outright neuron death and plaque accumulation. However, chronic overexpression leads to age-related axon degeneration and shortened lifespan.