Research in C. elegans shows the popular supplement engages longevity genes to increase lifespan and prevent the accumulation of toxic proteins linked to many age-related diseases
Small trial from the Buck Institute and UCLA succeeds using systems approach to memory disorders.
Our epigenome is a set of chemical switches that turn parts of our genome off and on and are impacted by environmental factors including diet, exercise and stress. Research at the Buck Institute reveals that aging also effects the epigenome in human skeletal muscle. The study provides a method to study sarcopenia, the degenerative loss of muscle mass that begins in middle age.
To tackle the rising prevalence of age-related diseases and the challenges and opportunities presented by a growing elderly population, the USC Davis School of Gerontology and the Buck Institute for Research on Aging today announced a joint Ph.D. program in the Biology of Aging, the first in the nation.
The major genetic risk factor for Alzheimer’s disease, present in about two-thirds of people who develop it, is ApoE4, the cholesterol-carrying protein that about a quarter of us are born with. But one of the unsolved mysteries of AD is how ApoE4 causes this risk. Researchers at the Buck Institute have found a link between ApoE4 and SirT1, an “anti-aging protein” that is targeted by resveratrol, present in red wine.
Have you ever wondered why young children can eat bags of Halloween candy and feel fine the next day – compared to adults who experience all sorts of agony following the same junk food binge? Evolution and a gene called Foxo may be to blame.
Research focused on the regulation of the adult stem cells that line the gastrointestinal tract of Drosophila suggests new models for the study of Barrett’s esophagus. Barrett’s esophagus is a condition in which the cells of the lower esophagus transform into stomach-like cells. In most cases this transformation has been thought to occur directly from chronic acid indigestion. A new study suggests a change in stem cell function for this transformation.
Mice suffering from age-related heart disease saw a significant improvement in cardiac function after treatment with the FDA-approved drug rapamycin for just three months. Research at the Buck Institute shows how rapamycin impacts mammalian tissues, providing functional insights and possible benefits for a drug that can extend lifespan in mice as much as 14 percent. Researchers at the Mayo clinic are now recruiting seniors with cardiac artery disease for a clinical trial involving the drug.
Scientists seeking to develop treatments for Huntington’s disease just got a roadmap that could dramatically speed their discovery process. Researchers at the Buck Institute have used RNAi technology to identify hundreds of “druggable” molecular targets linked to the toxicity associated with HD. The gene RRAS, involved in cell motility and neuronal development , was among the diverse range of modifiers identified. RRAS was revealed as a potent modulator of HD toxicity in multiple HD models.
Rapamycin, an FDA-approved immunosuppressant drug under study in aging research labs, improved function and extended survival in mice suffering from a genetic mutation which leads to dilated cardiomyopathy (DCM) and rare muscular dystrophies in humans. There are currently no effective treatment for the diseases, which include Emery-Dreifuss Muscular Dystrophy and Limb-Girdle Muscular Dystrophy.
Dietary restriction alone does not extend lifespan – at least in fruit flies. Flies, which share many genetic similarities with humans, need physical activity in order to live longer on a Spartan diet. If the same axiom holds true in humans, those practicing caloric restriction in hopes of living longer need to make sure they eat enough to avoid fatigue.
Researchers at the Buck Institute for Research on Aging have corrected the genetic mutation responsible for Huntington’s Disease (HD) using a human induced pluripotent stem cell (iPSC) that came from a patient suffering from the incurable, inherited neurodegenerative disorder. Scientists took the diseased iPSCs, made the genetic correction, generated neural stem cells and then transplanted the mutation-free cells into a mouse model of HD where they are generating normal neurons in the area of the brain affected by HD.
New research from the Buck Institute, built on spinal cord injury research, shows that modifying the scar tissue that develops following a stroke is a promising avenue for future treatments. The need for therapeutics for chronic stroke is compelling. There are 750,000 new strokes per year in the U.S., a leading cause of morbidity and mortality.
Alliance for Aging Research and the Buck Institute for Research on Aging urge support for research agenda aimed at extending healthy years of life. Nearly 70 prominent scientists endorse the plan and call for more federal funding.
About 18 million individuals undergo massage therapy annually in the U.S. Despite several reports that long-term massage therapy reduces chronic pain and improves range of motion in clinical trials, the biological effects of massage on skeletal tissue have remained unclear - until now.
The partnership, aimed at drug development, builds on observations that rapamycin extends healthy lifespan in several species.
When researchers at the Buck Institute dialed back activity of a specific mRNA translation factor in adult nematode worms they saw an unexpected genome-wide response that effectively increased activity in specific stress response genes that could help explain why the worms lived 40 percent longer under this condition. The study highlights the importance of mRNA translation in the aging process.
Buck Institute research in mice moves into preclinical stage; Buck working toward human trials.
Buck Institute study in Nature identifies novel metabolic signaling pathway in worms that coordinates the aging response to nutrient availability. Results provide missing piece of DR puzzle.
Basic Yellow 1, a dye used in neuroscience labs around the world, is a wonder drug for nematode worms. Thioflavin T extended lifespan in healthy worms by more than 50 percent and slowed the disease process in worms bred to mimic aspects of Alzheimer’s. The research could open new ways to intervene in aging and age-related disease.
Douglas Rosenberg sets $10 million goal for fund to develop treatment based on promising small molecule screening.
Buck Institute, Yale University and University of California, Berkeley scientists identify three caspase inhibitors that block HD-associated neuronal damage in cell culture; follow up experiments are underway in mice
Researchers at the Buck Institute for Age Research have discovered a novel way in which insulin affects cell metabolism and cell survival. Surprisingly the insulin signaling pathway, which is involved in aging, diabetes and stress response, is active at a deeper level of cell activity than scientists expected.
Researchers at the Buck Institute for Age Research have successfully used human induced pluripotent stem cells (iPSCs) to treat rodents afflicted with Parkinson’s Disease (PD). The research validates a scalable protocol that can be used to manufacture the type of neurons needed to treat the disease and paves the way for the use of iPSC’s in various biomedical applications.
Research reveals that an enzyme linked with many disorders - including cancer, stroke and rheumatoid arthritis - is also involved in the generation of the toxic fragments in Huntington's disease.
Brian K. Kennedy, PhD, has been appointed President and Chief Executive Officer of the Buck Institute for Age Research, effective July 1, 2010. Kennedy, who has earned an international reputation for his work in the basic biology of aging, comes to the Buck Institute from the University of Washington in Seattle where he most recently served in the Department of Biochemistry.
In a review appearing in Cell Metabolism, Buck Institute faculty Pankaj Kapahi , PhD, discusses activities related to TOR one of the key molecular players involved in increasing the healthy years of life via the process of dietary restriction.
Research on fruit flies provides new clues on the process - and open the door for future treatments for metabolic and eating disorders.
Research in rodents highlights the need for human clinical trials of antidepressants and other drugs shown to increase the growth of new neurons. Science at the Buck Institute for Age Research suggests a new strategy for treatment of stroke.
It is widely known that genetic mutations cause disease. What are largely unknown are the mechanisms by which these mutations wreak havoc at the molecular level, giving rise to clinically observable symptoms in patients. Now a new study using bioinformatics, reports the ability to predict the molecular cause of many inherited genetic diseases. These predictions have led to the creation of a web-based tool available to academic researchers who study disease.
This study, appearing in Cell, provides details of a causal relationship between diet and mitochondrial function. It also provides the first genome-wide study of how proteins are translated under dietary restriction in any organism. Flies fed a low protein diet live longer because their mitochondria function better. The molecular mechanisms involved are conserved among many species – making the research relevant for human aging and diseases such as obesity, cancer and diabetes.
Aging is the single largest risk factor for disease in developed nations. Yet, this biological process remains, for the most part, a mystery. Geroscience, a new scientific discipline established at the Buck Institute for Age Research, is aimed at solving that mystery and turning the risk factor on its head. The premise: slow aging and delay disease.
Our current health care crisis pales in comparison to the impending demographic "tsunami" that threatens to bankrupt our economy. A recent census report projects that within 10 years there will be more people aged 65 and older than children under 5 years of age. This is a first in human history and highlights the need for our nation to focus more attention and research dollars in finding ways to delay the aging process.
When cells experiencing DNA damage fail to repair themselves, they send a signal to their neighbors letting them know they're in trouble. The discovery, made at the Buck Institute for Age Research, shows that a process dubbed the DDR (DNA Damage Response) also controls communication from cell to cell. The research has implications for both cancer and aging.
The Buck Institute for Age Research has received a $1.6 million dollar "Eureka" grant from the National Institutes of Health to further its innovative research in Alzheimer's disease. The highly competitive grant was awarded to Buck faculty member and founding CEO Dale Bredesen, MD. Research in the Bredesen lab focuses on Alzheimer's as a potential "prionic" brain signaling disorder that impacts brain plasticity, rather than the current dogma that Alzheimer's is a disease of toxicity stemming from damage caused by sticky amyloid plaques that collect in the brain.
A protein that plays a key role in tumor formation, oxygen metabolism and inflammation is involved in a pathway that extends lifespan by dietary restriction. The finding provides a new understanding of how dietary restriction contributes to longevity and cancer prevention and gives scientists new targets for developing and testing drugs that could extend the healthy years of life.
When it comes to the aging process, yeast, nematode worms and fruit flies have more in common with humans than previously expected. In addition to highlighting the similarities between species, a large-scale human protein network reveals a complex web of interactions among the human equivalents of the many longevity genes found in simple-animals.
Is there something missing from the conventional theory that Alzheimer's is a disease of toxicity "“ based on the accumulation of sticky amyloid plaques in the brain? Research from the Buck Institute focuses on Alzheimer's as a nerve signaling disorder that occurs when there's an imbalance in the making and breaking of memories. The discovery of a naturally occurring brain protein, Netrin-1, offers a new target for therapeutics.
Cells shut down and stop dividing when their DNA is damaged, providing protection against cancer. However, a new study has found these cells also spew proteins into the cells' surrounding environment. The process, called cellular senescence, causes inflammation and sets up conditions that support the development of age-related diseases including, ironically, cancer.
Green technology now includes information technology infrastructure. The Buck Institute for Age Research has received LEED for Commercial Interiors Silver certification for a build out of new laboratory space, including an Innovation in Design Credit for Information Technology Infrastructure.
Determining chronological age is easy - count forward from birth. Establishing physiological age, especially in humans, is purely subjective - based on how someone looks or functions. Research in nematode worms could lead to the development of human biomarkers of aging, allowing us to track how we're withstanding the tests of time.
Buck Institute study shows mixed results for life extending properties of antioxidants. Consumers should use caution when taking supplements.
In a Nature Review, "Puzzles, promises and a cure for ageing", Buck Institute scientists Judith Campisi, PhD and Jan Vijg, PhD argue that there is no question human lifespan will almost certainly increase modestly over the coming decades. However, they critically analyze whether current knowledge has reached the state where postponing human aging and natural death for many decades, possibly indefinitely, is feasible.
A well-known growth factor has been shown to increase the growth of new neurons in mice induced to develop Parkinson's disease. The finding highlights a potential new therapy for the condition.
Who'd a thunk? Younger brains show evidence of more memory loss than those with Alzheimer's. But those younger brains are also making memories faster than they lose them. A Buck Institute study shows that normal memory loss is hyperactivated in Alzheimer's, pointing to AD as a syndrome affecting the plasticity or malleability of the brain.
Could people be tested for a possible risk factor for Parkinson's disease? A Buck Institute study suggests preventive treatment may be useful for those who have high levels of particular enzyme that regulates nerve activity in the brain
A Buck Institute study shows that depletion of the antioxidant glutathione leads to symptoms of Parkinson's disease in mice. The research also provides a new model for the study of the neurodegenerative disease while highlighting the role of aging in disease development.
Buck Institute study shows potential of human protein to lessen severity of Alzheimer's disease.
Nematode worms treated with lithium show a 46 percent increase in lifespan, raising the tantalizing question of whether humans taking the mood affecting drug are also taking an anti-aging medication.
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