Articles tagged with Progeria
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Researchers have identified a 'longevity gene' from supercentenarians that can slow down heart aging in a progeria model. The gene helps keep the heart and blood vessels healthy during aging, reducing signs of aging and fibrosis in Progeria patients.
A new study found that miR-145-5p and miRNA-27b-3p interfere with fat cell formation in children with Hutchinson-Gilford progeria syndrome, a rare and fatal premature aging disorder. These microRNAs silence genes required for fat cell growth and function, suggesting they could be a promising therapeutic strategy to restore fat tissue.
Two new studies from Karolinska Institutet investigate how somatic mutations in muscles and blood vessels affect ageing. The results show that such mutations can reduce muscle strength and accelerate blood vessel ageing.
Researchers have discovered that nicotinamide riboside supplementation significantly improves NAD+ levels, reducing arterial stiffness, skin ulcer area, and kidney dysfunction. This breakthrough offers new hope for patients with Werner syndrome who lack effective treatment options.
Researchers identified a protein that could improve the cardiovascular health of patients with progeria, a rare genetic disorder. The discovery provides promising insights into potential treatments targeting cardiovascular complications in HGPS.
A team of researchers has identified the activation of the YAP/TAZ pathway as a major contributor to atherosclerosis in patients with Hutchinson-Gilford progeria syndrome. This discovery sheds light on the vascular problems faced by HGPS patients and opens up potential new avenues for treatment.
Researchers at CNIC have identified endothelial-to-mesenchymal transition as a novel mechanism in premature atherosclerosis in progeria. The study proposes a new therapeutic target for this disease and highlights the importance of investigating rare diseases like progeria.
Researchers have defined what a premature aging disease is and developed tools to diagnose progeria patients, allowing them to identify new syndromes. The study also identified correlations between progeroid syndromes and other conditions, providing a significant step forward in understanding premature aging.
Researchers investigated hepatic hydrogen sulfide production in a mouse model of Hutchinson-Gilford Progeria Syndrome (HGPS) and found reduced H2S levels in RC-fed mice, with partial rescue on high-fat diet. This study suggests that accelerated aging in HGPS may be partially explained by reduced hepatic H2S levels.
A new study suggests that prelamin A, a precursor of lamin A, accumulates with age and may drive normal aging. Researchers propose this protein as a target for intervention strategies to extend healthspan and lifespan.
Scientists have identified long interspersed nuclear element-1 (L1) RNA as a promising new target for treating progeroid syndromes. Increased L1 RNA expression in cells from patients with these disorders led to deactivation of an enzyme, causing cell aging.
Researchers identify LINE-1 RNA as a key player in premature aging, revealing its role in progeria and potential therapeutic targets. By inhibiting LINE-1 RNA, scientists reverse signs of aging and extend lifespan in mice.
Researchers successfully used DNA-editing to extend the lifespan of mice with progeria by correcting the accelerating aging disorder. The treatment restored normal DNA sequences in various organs and improved mouse lifespans from seven months to nearly 1.5 years.
Researchers developed an advanced blood vessel model to study progeria, a devastating genetic disease. The model shows that the endothelium, not just smooth muscle cells, plays a crucial role in progeria symptoms, and dynamic 3D models are necessary to understand its effects.
Researchers at Karolinska Institutet identified antisense oligonucleotide therapies as a new possible treatment option for progeria. In mice and human cells, the treatments showed promising results by reducing telomeric non-coding RNA and improving cell division.
Researchers have discovered a new molecular mechanism involved in premature atherosclerosis in mice with Hutchinson-Gilford progeria syndrome. The study identifies tauroursodeoxycholic acid as a potential therapeutic target that slows the progression of atherosclerosis and extends lifespan in progeroid mice.
A new gene therapy using CRISPR/Cas9 targets the accumulation of toxic proteins in progeria syndrome, a rare genetic disorder. The therapy improves health and life span in mice, providing insight into molecular pathways involved in accelerated aging.
Researchers have generated the first mouse model of atherosclerosis accelerated by progerin, a protein causing Hutchinson-Gilford syndrome. The study identifies vascular smooth muscle cells as a key target for treating premature atherosclerosis in progeria.
Scientists at the Salk Institute have discovered an errant protein process in a rare genetic disorder that could help healthy people live longer. The study found rapid protein turnover and enlarged nucleoli in progeria cells, which may serve as biomarkers for aging.
Biomedical engineers have grown miniature human blood vessels exhibiting symptoms of Hutchinson-Gilford Progeria Syndrome, an extremely rare genetic disease. The technology will help doctors screen potential therapeutics more rapidly, with the goal of creating a personalized screening platform.
Scientists at Houston Methodist have developed a technology that can rejuvenate human cells by lengthening telomeres, the timekeepers of chromosomes. This breakthrough has the potential to improve cell function and extend lifespan in individuals with progeria, a rare condition marked by rapid aging.
Researchers at the Salk Institute have discovered that intermittent expression of genes normally associated with an embryonic state can reverse the hallmarks of old age. This approach resulted in the rejuvenation of mice with a premature aging disease, countering signs of aging and increasing their lifespan by 30%. The early-stage work...
Progeria, a rare genetic disease, is characterized by an elevated risk of arrhythmias and premature death due to anomalies in the transmission of electrical signals in the heart. The study reveals that mislocalization of connexin 43 reduces connectivity between cardiomyocytes, increasing the risk of arrhythmias.
A new study from the University of Maryland found that methylene blue can almost completely repair defects in cells with progeria and restore healthy cell function. The compound also repaired age-related damage to healthy cells, suggesting its potential as a treatment for both progeria and normal aging.
A study by University of Maryland researchers has identified a toxic protein that damages muscle cells inside the arteries of children with progeria, a rare genetic disorder. The discovery may help explain how cardiovascular disease develops in people aging normally and could lead to new treatments for the condition.
CNIC researchers have identified a possible treatment to block the deposition of calcium in arterial walls, a key symptom of premature aging disease. Chronic treatment with pyrophosphate inhibits calcium deposition, which is accelerated in mice with Hutchinson-Gilford progeria syndrome.
A new study offers promising hope for treating progeria by targeting the enzyme ICMT, which causes premature aging. Researchers have successfully tested an ICMT inhibitor on mice, reducing or blocking the development of progeria symptoms and increasing cell growth.
Research identifies epigenetic changes in Hutchinson-Gilford Progeria and Werner Syndrome patients, revealing a potential role for DNA methylation in premature aging diseases. No genetic cause has been previously associated with the onset of these conditions.
Researchers have discovered that farnesyl transferase inhibitors significantly slow the progress of progeria, a rare and lethal genetic disorder. The use of these inhibitors has been shown to slow bone loss and blood vessel blockage in children with progeria.
A clinical trial demonstrates significant improvements in Progeria children's weight gain, bone structure, and cardiovascular system after receiving a farnesyltransferase inhibitor. The treatment, originally developed for cancer, has shown promising results in slowing down the progression of the disease.
Researchers at A*STAR's Institute of Medical Biology found that reducing SUN1 levels in mouse models doubled the life spans of those with progeria and tripled it for those with Emery-Dreifuss muscular dystrophy. This discovery opens up a possibility for therapeutic use of reduced SUN1 levels for other forms of heart disease.
A study led by Durham University has identified a potential drug therapy for premature ageing diseases, including Hutchinson Gilford Progeria Syndrome. The treatment, N-acetyl cysteine (NAC), controlled oxidative stress and DNA damage in cells, suggesting a possible model for understanding processes that cause us to age.
Researchers have developed a new animal model to study Progeria and tested a gene therapy that significantly extended the lifespan of mice. The treatment, using 'vivo-morpholino' antisense oligonucleotide technology, reduced progerin production and improved various parameters related to the disease.
A new study by NIH researchers reveals the interaction between telomeres and a toxic protein called progerin that triggers both premature aging syndrome and normal cellular aging. Shortened telomeres lead to increased production of progerin, causing cell damage and activation of programmed aging.
A new study identifies a mutation underlying accelerated-aging disease, providing key insights into normal human aging. The research highlights the importance of the nuclear envelope in the aging process.
Researchers have developed a genetic model of premature aging disorders in zebrafish, which can be used to screen and develop compounds to treat these conditions. The model reveals that a specific gene mutation leads to accelerated aging in the fish, providing new insights into age-related diseases.
Scientists at Salk Institute successfully generated induced pluripotent stem cells from patients with Hutchinson-Gilford Progeria Syndrome, a rare disorder that accelerates aging. The cells displayed signs of vascular aging and were differentiated into smooth muscle cells that showed premature aging phenotypes.
Scientists have created the world's first human cell model of progeria, a rare genetic disease causing severe premature ageing in children. The model reveals defects in mesenchymal stem cells and vascular smooth muscle cells that exacerbate symptoms of ageing.
A study published in Developmental Cell sheds light on Hutchinson-Gilford Progeria Syndrome, a rare genetic disease causing premature aging. Researchers discovered that defects in the extracellular matrix and Wnt signaling pathway contribute to progeria's characteristic symptoms.
A study has discovered that progerin, the protein responsible for Progeria, is present in the vasculature of the general population and increases with age. Researchers found that progerin levels in coronary arteries increased by an average of 3.3% per year between one month and 97 years.
Researchers at UT Southwestern Medical Center have identified distinct traits in patients with atypical progeroid syndrome (APS), a rare premature aging disorder. The study found that APS patients exhibit unique clinical features, metabolic abnormalities, and delayed onset of symptoms, potentially explaining their longer lifespan.
The gene responsible for Progeria has led to a promising experimental drug being evaluated in 28 children with the disease. Researchers have pinpointed the genetic mutation and identified an effective therapy, potentially treating this fatal disorder.
Researchers have found that an experimental anti-cancer drug can prevent and reverse cardiovascular damage in a mouse model of progeria, a rare genetic disorder causing human premature aging. The study suggests that the drug may also have potential in treating other forms of coronary artery disease.
Researchers found that both farnesylated and non-farnesylated progerin can cause symptoms of Hutchinson-Gilford progeria syndrome (HGPS), a rare childhood disorder resembling premature aging. The study uses a new mouse model to challenge the effectiveness of inhibitors of farnesylation as a potential therapy.
Researchers discover that infants who died of mysterious illnesses had unique LMNA gene mutations, leading to increased production of the bad protein lamin A. Treating these cells with a drug meant for progeria patients showed promising signs of improvement.
Researchers have identified a mutant protein as a key culprit molecule in causing heart disease, including atherosclerosis, which is a leading cause of heart attacks and strokes. The study also sheds light on the progression of progeria, a rare genetic condition that accelerates aging in children.
A new UCLA study published in Science suggests that a farnesyltransferase inhibitor (FTI) may be useful in treating progeria, a genetic disease causing accelerated aging in children. The majority of FTI-treated mice showed improvements in body weight, bone integrity, grip strength, and survival compared to untreated control mice.
Researchers discover that mutant lamin A proteins interfere with key controls of gene expression and cell cycle, leading to rapid aging in HGPS patients. The study suggests that similar missteps may be part of normal human aging.
Researchers found that farnesyl transferase inhibitors can normalize abnormal nuclei in progeria cells. The treatment targets a genetic mutation causing lamin A protein production issues.
Researchers at UCLA used a drug to block mutant proteins from deforming cell nuclei, significantly reducing misshapen nuclei in human cells. The findings offer new clues into how progeria develops and could lead to treatment with new drugs for related disorders like osteoporosis.
A study published in PNAS suggests that farnesyltransferase inhibitors (FTIs) may reverse nuclear structure abnormalities in progeria cells. Researchers treated progerin-carrying skin cells with FTIs, reducing cell blebbing and improving cellular function.
Researchers have found that certain anti-cancer drugs, known as FTIs, can block biochemical processes causing progeria's symptoms. The collaboration has shown a strong positive effect on progeria patients' cells.
Children with Progeria have lower levels of HDL cholesterol and adiponectin, contributing to accelerated plaque formation. The study aims to better understand atherosclerosis in the aging population and find treatments for this rare genetic disorder.
A new study reveals that children with Progeria experience progressive nuclear structure and function defects due to the accumulation of defective Lamin A protein. The findings provide critical insights into the cause of heart disease and cellular aging in this fatal disease.
Researchers have developed a new mouse model that mimics progeria, a rare condition characterized by accelerated aging. The mouse model shares symptoms with human patients, including growth retardation, skin thinning, and premature death, providing valuable tools for studying the aging process.
Researchers have identified the Progeria gene, which may lead to answers about natural aging and cardiovascular disease. The discovery gives hope to children with Progeria, who die at an average age of 13 due to complications from accelerated aging.
A France-based research team has discovered the gene responsible for Hutchinson-Gilford Progeria, a disease that causes young victims to age five to ten times faster than normal. The discovery is a critical step toward developing therapies for the disorder and programs to screen individuals for the defective gene.
Hutchinson-Gilford progeria syndrome affects 1 in 8 million newborns worldwide and is characterized by accelerated aging. The researchers identified a single-letter misspelling in the LMNA gene as the cause of this disorder.
Researchers found progeria cells have low catalase and glutathione peroxidase activity, making it hard to remove toxic peroxides. Reintroducing these enzymes could halt or reverse the problem using adenovirus gene transfers.