Articles tagged with Amyloidosis
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Scientists used Exploratory Investigational New Drug (ExpIND) to evaluate four 18F-labeled imaging agents in patients with Alzheimer's disease, identifying the best detector of amyloid plaque deposits. The study suggested that ExpIND could speed up the development of new radiopharmaceuticals while ensuring patient safety.
Researchers confirm that Pittsburgh Compound-B binds to beta-amyloid deposits found in Alzheimer's brains, enabling definitive diagnosis. The finding aids in early detection and treatment of the disease.
Researchers engineered mice to overexpress ABCA1, reducing amyloid deposition in the brain, a hallmark of Alzheimer's disease. This study provides new insights into the disease's pathophysiology and potential therapeutic targets.
Researchers have made significant breakthroughs in Alzheimer's disease research, identifying A
Researchers found that high-dose chemotherapy and blood stem cell transplantation can result in long-term survival for patients with primary systemic light chain (AL) Amyloidosis. The median survival for all 80 patients was 57 months, with 18 still alive 10+ years after treatment.
Researchers from Boston University Medical Center successfully treat patients with immunoglobulin-light chain amyloidosis who did not respond to initial treatment. A tandem approach of high-dose chemotherapy and blood stem cell transplantation shows improved overall survival and quality of life for these patients.
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.
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.
Researchers found high levels of zinc in deposits in the eye associated with age-related macular degeneration. The discovery may facilitate the development of effective treatments for this leading cause of blindness among the elderly.
Researchers found that mice born to mothers with senile amyloidosis exhibited elevated levels of amyloid fibrils, accelerating disease onset. The presence of fibrils in the milk of affected mothers was confirmed, demonstrating transmission via nursing.
A genetic mutation in a heart protein has been identified as a risk factor for sudden infant death syndrome (SIDS) in African American infants. Diabetic patients may benefit from a nerve survival protein called GDNF to treat gastrointestinal disorders related to diabetes.
Researchers have found that a specific immunization strategy targeting Abeta42 or Abeta40 can prevent amyloid deposition in mice, suggesting an effective approach for preventing Alzheimer's disease. However, this method may not be effective once existing deposits are established.
Researchers discover that preventing amyloid deposition may be easier than curing established Alzheimer's disease through an immunization strategy targeting Abeta42. Additionally, a study finds that pre-treatment of patient T cells with IL-10 and vitamin D3 can overcome glucocorticoid resistance in asthma patients.
Researchers at the University of Pittsburgh discovered a brain imaging method to monitor Alzheimer's disease progression non-invasively using Pittsburgh Compound-B. This breakthrough allows for early diagnosis and monitoring of amyloid plaque deposits, which are thought to cause brain cell death.
A new study suggests that scintigraphy using radioactive isotope (99mTc-DPD) can help distinguish between hereditary and acquired forms of cardiac amyloidosis, two conditions with different treatment options. The test shows promise in reducing misdiagnosis and improving patient outcomes.
Studies using transgenic mice reveal impaired amyloid-beta clearance leads to vascular damage and neuroinflammation in the brain. This process appears to contribute to the progression of Alzheimer's disease, suggesting novel therapeutic targets to reduce blood vessel-associated Aβ deposition.
Researchers have discovered a new enzyme family that plays a role in Alzheimer's disease, generating toxic molecules called amyloid-beta peptides. The study uses genetically-engineered mice to show that the toxic activity of this enzyme can be separated from its other benign activities.
A study found that short heparansulfate chains trigger amyloid deposits, which are associated with Alzheimer's disease. The research suggests that short segments of sugar chains may be useful in developing new drugs for the condition.
Scripps Research scientists identified that certain tissues are more susceptible to amyloid plaques due to their ability to efficiently release misfolded protein. The study found that cells secreting proteins into these tissues secrete the bad proteins most efficiently, making them a key factor in tissue selectivity.
Researchers at Duke University are using advanced atomic force microscopy techniques to study the interactions of individual amyloid protein molecules, which may hold key to preventing plaque formation. The goal is to develop a better understanding of amyloid aggregation and its role in neurodegenerative diseases.
Mice raised in an enriched environment with running wheels and toys showed reduced beta-amyloid deposits and increased enzyme activity. They also exhibited improved genes involved in learning, memory, brain cell survival, and blood vessel growth.
Research suggests that statins can increase 'healthy' (non-amyloidogenic) cleavage of amyloid precursor protein (APP), potentially protecting against Alzheimer's disease. In a study, two different statins increased healthy cleavage of APP in mouse neuroblastoma cells.
Researchers have identified a new species of amyloid β-peptide, Aβ46, which is 46 amino acids long and produced by γ-secretase at a novel cleavage site. This discovery may provide new insights into the mechanism of Alzheimer's disease and open up avenues for treatment and prevention.
Apolipoprotein E is responsible for converting harmless amyloid-beta protein into toxic filamentous amyloid, a major hallmark of Alzheimer's disease. Mice with the gene showed memory deficits only when it was present.
Researchers discovered that apolipoprotein E and clusterin proteins can delay amyloid plaque formation in mice with Alzheimer's-like brain damage. The findings imply that these proteins cooperate to suppress Abeta protein levels and deposition, paving the way for future drug or gene therapy treatments.
Researchers have discovered that smaller protein structures called protofibrils are more toxic to cells than mature fibrils in type II diabetes and other age-related diseases. The study suggests that targeting earlier stages of protofibril formation may be a more effective approach to developing treatments.
The study reveals that renal amyloidosis is associated with a poor prognosis in patients with Familial Mediterranean Fever. AA amyloidosis is a chronic and fatal disease marked by the deposit of amyloid fibrils in the kidney, leading to organ dysfunction and death.
Researchers have discovered a new anti-inflammatory drug, NCX-2216, that effectively removes excess amyloid protein from the brains of mice with Alzheimer's-like memory disorders. The nitro-NSAID also activates immune cells called microglia, which may help remove amyloid before it hardens into toxic plaques.
A new drug, CPHPC, has been developed to remove a blood protein linked to amyloidosis, a disorder that claims 1,000 UK lives annually. The drug blocks SAP proteins from sticking to amyloid fibers, speeding up their removal and offering potential treatment for Alzheimer's and diabetes.
Researchers at Mayo Clinic have successfully bred mice with both amyloid plaques and neurofibrillary tangles, the key pathologic hallmarks of Alzheimer's disease. The double transgenic mouse model provides a more complete representation of human AD and will enable researchers to test therapies aimed at preventing or halting progression.
Scientists have discovered a vaccine that may prevent and treat Alzheimer's by blocking the production of toxic amyloid ß peptides, which accumulate in the brain and cause dementia. The vaccine has shown promise in removing amyloid plaques and preventing learning impairment in transgenic mice, paving the way for potential human trials.
A team of researchers found that the protein alpha1-antichymotrypsin doubles the accumulation of Alzheimer's disease-associated amyloid plaque in mice brains, indicating a potential therapeutic target. The study suggests that reducing or inhibiting this protein's activity could help prevent plaque formation and brain damage.
Thalidomide demonstrates potential activity in multiple myeloma, primary amyloidosis, metastatic colorectal cancer, and acute myeloid leukemia, with notable improvements in patient survival rates and side effects observed.
Researchers identified LRP-1 as a key molecule in removing beta amyloid protein from the brain through blood circulation. In healthy mice, blood vessels efficiently clear amyloid peptide, whereas impaired LRP-1 function can lead to plaque accumulation and neurodegeneration.
Researchers discovered a direct link between apoE and cerebral amyloid angiopathy (CAA), a leading cause of bleeding strokes in the elderly. Decreasing apoE expression may inhibit CAA buildup, lowering the risk for cerebral hemorrhage.
Researchers at the University of Kentucky have discovered a new potential target for compounds that may treat or prevent Alzheimer's disease. The receptor RAGE interacts with amyloid fibrils, accelerating fibril formation and inducing cellular dysfunction.
A University of Colorado study identified deposits of beta amyloid in the brains of wild, aging landlocked salmon, sparking new ideas about human aging and Alzheimer's disease. The study found that while brain regions responsible for memory and navigation were affected, other areas continued to function normally.
Researchers found that apoE4, a high-risk version of the lipoprotein, directly promotes the development of neuritic plaques in the brain by enabling amyloid-beta to form into hair-shaped fibrils. ApoE3 had less damaging effects. The study used a mouse model and showed that apoE interaction with amyloid-beta leads to neurodegeneration.
Scientists have created a genetically-engineered mouse model with human tau genes, allowing for the study of tau-containing lesions in various brain disorders. The new model shows abnormal tau filaments accumulating in nerve cells, similar to those found in Alzheimer's disease.
A new imaging method is being developed to show images of plaque deposits in the brains of Alzheimer's patients as the disease progresses. The technology uses technetium-based probes to detect amyloid plaque deposits, which could allow for definitive diagnosis before death.
A novel gene, BRI, located on chromosome 13 has been identified as responsible for familial British dementia, a rare inherited disease that causes progressive dementia and spasticity. The discovery provides new clues to the abnormal changes in the brain that lead to dementia.
Researchers identified a novel human gene, BRI, that causes an unusual form of hereditary dementia. The discovery provides new insights into the disease and may lead to the development of a blood test to detect the mutation.
Researchers found a new mechanism explaining how Alzheimer's disease damages the brain by producing hydrogen peroxide from oxygen, a toxic agent that can cause brain damage. The discovery provides a potential target for new drugs to treat Alzheimer's, which affects four million Americans.
Scientists have created a synthetic peptide that blocks the formation of amyloid plaques in the brain, destroying existing plaques and preventing nerve cell death. This breakthrough may lead to a new therapy for Alzheimer's disease and other diseases caused by defective protein folding.
Researchers found increased levels of butyrylcholinesterase (BChE) in brains with compact and insoluble beta-amyloid plaques, a hallmark of Alzheimer's disease. BChE may play a role in transforming benign amyloid protein deposits into the disease-causing plaques.
Researchers found that a gene linked to family-inherited Alzheimer's accelerates amyloid peptide production and plaque formation. The study suggests that early changes can be targeted with drugs to slow or prevent the disease.
Researchers discovered a way to disrupt the aggregation of proteins that form poisonous plaque deposits in Alzheimer's patients. By synthesizing specific inhibitor molecules, they successfully blocked the toxicity of beta amyloid proteins, potentially leading to new treatments for the devastating disease.