Scientists discovered that increasing EphB2 levels can fix memory problems caused by amyloid proteins in a mouse model of Alzheimer's disease. The study found that blocking amyloid proteins from binding to EphB2 and enhancing its functions may be beneficial for AD treatment.
Researchers at Gladstone Institute of Virology and Immunology discover how HIV promotes the death of CD4 T cells by infecting them with a failed form of viral replication. This process leads to the depletion of these critical immune cells, ultimately causing AIDS.
Gladstone scientists discovered a process by which Alzheimer's disease spreads through the brain, starting in vulnerable regions like the entorhinal cortex. The study suggests targeting this region could be an effective therapeutic approach.
Researchers at the Gladstone Institutes have discovered that ApoE4 causes learning and memory deficits by impairing GABAergic interneuron function. The study found that apoE4-dependent deficits were rescued by pentobarbital, a compound that enhances GABA action.
Researchers found that an enzyme associated with fat storage in liver cells is required for HCV infectious activity. DGAT1 inhibitors may be effective against HCV, with several already in early clinical trials to treat obesity-associated diseases.
Researchers found that tau acetylation contributes to Alzheimer's disease and other neurodegenerative diseases. Inhibiting tau acetylation may be a new approach for reducing tau-related pathology.
Scientists have discovered a strategy to prevent Alzheimer's-associated traffic jams in the brain by reducing tau protein levels. By blocking amyloid beta proteins, which disrupt transport of vital cargoes between brain cells, researchers found that tau reduction effectively prevents such traffic jams.
Researchers at Gladstone Institutes found a way to make beating heart cells from body's own cells, helping to regenerate damaged hearts. The new method directly reprograms structural cells called fibroblasts into cardiomyocytes without needing stem cell state.
Researchers at Gladstone Institutes establish a connection between brain circuits and Parkinson's disease symptoms, identifying a potential treatment strategy. By activating specific pathways, they can mimic Parkinson's-like symptoms and even restore motor function in mice with dopamine deficiency.
The collaboration aims to identify genes and novel drug targets related to the onset and progression of Huntington's disease. The team will use induced pluripotent stem cells from patients with HD to screen for drugs that might delay, prevent, or reverse the devastating condition.
Researchers at the Gladstone Institutes discovered that SIRT3 plays a crucial role in regulating fatty acid oxidation and identified it as a potential therapeutic target. Mice lacking SIRT3 exhibited impaired fat burning and increased levels of fat and triglycerides, highlighting the enzyme's importance in energy metabolism.
Researchers at Gladstone Institute of Cardiovascular Disease discovered that DGAT1, an enzyme involved in fat storage, protects against diet-induced inflammation and insulin resistance. Enhancing DGAT1's capacity in macrophages may hold therapeutic promise for preventing obesity-related diseases.
Researchers found that mislocation of TDP-43 from the nucleus to the cytoplasm causes neurodegeneration associated with ALS and frontotemporal lobar degeneration. The study used a model system to investigate the effects of mutant TDP-43 on neurons.
Researchers at the Gladstone Institutes have discovered surfen, a small molecule that inhibits HIV's ability to bind to cells and enhance infection. The discovery could lead to new treatments for HIV, potentially reducing transmission rates through sexual contact.
Researchers at Gladstone Institute of Neurological Disease have discovered that two main causes of AD, amyloid-beta peptides and apolipoprotein E4, impair the growth of new neurons born in adult brains. Drug treatments can normalize their development even in the presence of these factors.
Scientists at Gladstone Institute of Cardiovascular Disease and Stanford University School of Medicine are developing induced pluripotent stem cells to repair damaged heart muscle. The $10 million, 7-year project aims to identify and characterize progenitor cell lines and develop new clinical strategies for regenerative therapies.
The Gladstone Institute of Cardiovascular Disease has been awarded a $10 million grant to investigate the genetic causes of congenital heart disease. The team will use genome-mapping techniques to understand how regulatory networks control heart development and aim to identify genes that turn on or off during heart formation.
The Gladstone Institute of Neurological Disease and partners will use induced pluripotent stem (iPS) cell technology to develop human neurons with Huntington's disease characteristics, offering hope for new treatments. The goal is to understand the molecular differences between mice and humans that lead to ineffective therapies.
Gladstone scientists have found the first genetic link between reptile and human heart evolution, linking protein Tbx5 to the development of four-chambered hearts in turtles and humans. The study sheds light on the evolution of warm-bloodedness and provides insights into congenital heart disease.
Researchers at Gladstone Institute discovered a key switch, microRNA-145 (miR-145), to turn stem cells into muscle cells that reside in blood vessel walls. This finding suggests restoring miR-145 activity could prevent artery narrowing and vessel disease.
Researchers at Gladstone Institutes have found a key factor controlling HIV latency, which could lead to new strategies for clearing the virus. The discovery involves DNA methylation and a host protein called MBD2, and offers hope for future therapies to reactivate latent HIV.
Researchers have identified three genetic factors that can turn non-muscle cells into beating heart cells, providing a significant breakthrough in understanding how to repair damaged hearts. The discovery could lead to the development of new therapeutic approaches using stem cells.
The new center aims to prevent, treat, or cure Huntington's disease by 2020 through cutting-edge research and collaboration with pharmaceutical companies. Investigators will focus on identifying potential drug targets and developing innovative technologies to modulate the disease.
Researchers identified acyl CoA: monoacylglycerol acyltransferase 2 as a critical enzyme in fat absorption. In mice genetically modified to lack this enzyme, high-fat diets failed to induce obesity and related symptoms.
Researchers at the Gladstone Institutes have identified a complex signaling process that governs heart cell expansion and division. The study shows that cardiac fibroblasts send signals to cardiomyocytes to divide or grow, which could lead to regenerative therapies after heart attacks.
Gladstone scientists discovered that the DGAT1 enzyme plays a crucial role in regulating retinoic acid levels in the skin. Mice lacking this enzyme experienced increased retinoic acid levels, leading to skin sensitivity and hair loss, which could be prevented by restricting retinol intake.
Researchers at the Gladstone Institute of Neurological Disease discovered that collagen VI protects brain cells against amyloid-beta proteins, which are widely thought to cause Alzheimer's disease. The study found that increased collagen VI expression can effectively protect neurons against Aβ toxicity.
Researchers have identified a single microRNA, miR-138, critical to the development of heart chambers in zebrafish. This discovery may provide new approaches for treating congenital heart defects. The study showed that miR-138 regulates numerous gene functions and is required during a specific developmental window.
Scientists at Gladstone Institute of Neurological Disease have identified a new approach to destroy amyloid-beta proteins, which are linked to Alzheimer's disease. By reducing the natural inhibitor cystatin C, they can unleash potent enzyme cathepsin B to clear AB proteins from the brain.
Researchers discovered specific fatty acids contributing to Alzheimer's disease progression and proposed a therapeutic strategy by inhibiting an enzyme regulating fatty acid levels. Lowering the enzyme's activity improved cognitive deficits in mouse models.
Dr. Shinya Yamanaka's laboratory has eliminated the need for a virus to introduce genes into adult cells, improving the safety of induced pluripotent stem (iPS) cell technology for regenerative medicine applications.
Researchers at Gladstone Institutes have discovered a gene, Apobec3, that controls the production of antibodies neutralizing retroviruses, including HIV. This finding may lead to the development of an HIV vaccine by eliciting neutralizing antibodies.
Researchers found that microRNA miR-126 regulates vascular development, structure, migration, proliferation and survival of endothelial cells. The study provides clues to potential therapeutic targets for diseases impacted by the vascular system.
The Gladstone Institute of Cardiovascular Disease has developed WikiPathways, an open collaborative platform for curating biological pathways. This tool enables easy participation from the scientific community in peer review, editorial curation, and maintenance of pathway content.
Researchers found a faster disease course and increased HIV entry in patients with the apoE4 allele. The study suggests apoE4 may have clinical applicability in treating both Alzheimer's and HIV diseases.
Researchers at Gladstone Institutes have identified genes responsible for fat storage in cells, which may lead to new understanding and potential treatments for obesity, diabetes, and heart disease. The study found that ~1.5% of all genes function in lipid-droplet formation and regulation.
Researchers at Gladstone Institutes have found that modulating enkephalin peptides in the brain may reduce cognitive deficits seen in Alzheimer's disease. Increased levels of preproenkephalin mRNA and enkephalins in brain regions affected by AD were observed, suggesting a potential new therapy target.
Researchers at Gladstone Institutes have identified two microRNAs, miR-1 and miR-133, which play a crucial role in controlling the differentiation of pluripotent embryonic stem cells into cardiac muscle. These findings provide insight into fine-tuning cellular processes and may lead to new treatments for heart-related diseases.
Researchers at Gladstone and UCSF found that growth hormone therapy stimulates the production of vital T-cells, leading to increased thymic mass and improved immune function. The study suggests that this treatment could help HIV-infected patients rebuild their compromised immune systems.
Acclaimed stem cell researcher Shinya Yamanaka successfully reprograms human adult cells into pluripotent stem cells capable of developing into any cell type. This breakthrough accelerates the pace of stem cell research and holds promise for generating alternative sources of human pluripotent stem cells.
Researchers found that high levels of Amyloid-beta induce seizure-like activity in learning and memory centers, leading to cognitive impairments. The study provides new insights into the development of Alzheimer-related cognitive decline and potential therapeutic strategies.
Deepak Srivastava, GICD Director, received the prestigious E. Mead Johnson Award for his work in understanding normal and abnormal cardiogenesis. His research focuses on using knowledge of cardiac developmental pathways to devise novel therapeutics for human cardiac disorders.
Scientists at Gladstone Institutes have discovered a new strategy to prevent acute and chronic brain diseases by reducing tau protein levels. The study shows that mice lacking tau protein can resist seizures and Alzheimer's-related memory loss.
Researchers at Gladstone Institute of Cardiovascular Disease identified a critical genetic factor, microRNA miR-1-2, that regulates heart form and function. The study found that deletion of this microRNA causes defects in heart growth, function, and electrical conduction, potentially leading to new treatments for cardiovascular diseases.
Researchers from Gladstone Institutes have gained a better understanding of the use of stem cells to generate replacement cells for damaged heart muscle and vessels. The study highlights several challenges ahead, including guiding stem cells into cardiac lineage and integrating them safely within patients' heart tissue.
Researchers have discovered that neurons can produce a key protein linked to Alzheimer's disease under certain conditions. The study uses a unique mouse model to show that apoE production is regulated by the brain's response to injury, shedding light on the mechanisms underlying this complex disorder.
The J. David Gladstone Institutes will develop and implement a three-year, stem cell-specific curriculum for 10 postdoctoral fellows using the first third of $2.4 million grant. The program aims to educate scholars from various scientific backgrounds in stem cell biology and disease.
Scientists at Gladstone Institutes have successfully imaged the native state of apoE4, a key protein in Alzheimer's and cardiovascular diseases. This breakthrough has significant implications for developing future therapeutic interventions by providing a complete understanding of the protein's configuration.
Researchers at Gladstone Institutes have made a breakthrough discovery about the role of miRNA-1 in the early stages of heart development. They found that miR-1 helps determine heart progenitor cells and maintain them until later embryonic stages, which could lead to new strategies for cardiac regenerative medicine.
Researchers found that specific fragments of the apoE4 protein are neurotoxic and accumulate in mitochondria, leading to neuronal death characteristic of Alzheimer's disease. Blocking interaction of these fragments with mitochondria may be a potential new strategy for inhibiting detrimental effects.