Adult stem cells adjust proliferative activity in response to various signals through intracellular calcium signaling, revealing a master regulator of stem cell activity. Elevated Ca2+ levels regulate stem cell division and growth in response to L-glutamate, infection, and tissue damage.
Research reveals that dietary restriction enhances the expression of circadian clock genes in fruit flies, improving fat metabolism and extending lifespan. The study suggests a potential target for drug development to promote healthy aging.
Researchers at the Buck Institute have identified 238 genes that, when removed, increase the replicative lifespan of yeast cells. The study also reveals a link between these genes and caloric restriction, DNA damage control, and age-extending pathways in higher organisms.
Researchers discovered rapamycin prevents Parkinson's disease by boosting cellular clean-up via up-regulation of a protein called TFEB, increasing lysosomal autophagy and mitochondrial biogenesis. This breakthrough challenges current dogma and presents new opportunities for drug discovery.
The Buck Institute joins forces with Chilean researchers to tackle the growing crisis of an aging population. The Center for Geroscience, Brain Health and Metabolism will focus on understanding the interface between aging and neurodegenerative diseases.
Researchers at the Buck Institute found that increased free radicals in mice accelerated wound healing in young animals but led to thin skin and poor wound healing as they aged. This study sheds light on current discrepancies regarding the role of free radicals in the aging process.
Research demonstrates impaired activation of mitochondrial energy metabolism in patients with type 2 diabetes, leading to decreased insulin secretion. A novel fluorescence microscopic assay reveals a subtle disharmony between bioenergetic supply and demand pathways, suggesting a shift towards systems-level approaches to fight the disease.
Researchers found that low-dose lithium reduced involuntary motor movements in Parkinson's disease mice, boosting dopamine synthesis via inhibition of calpain-1. This study adds to evidence that low-doses of the psychotropic drug could benefit patients suffering from the incurable condition.
Researchers found that intermittent dosing with rapamycin selectively breaks the cascade of inflammatory events triggered by cellular senescence, providing proof-of-principal for a new treatment paradigm. The study shows that once disrupted, it takes time for the inflammatory loop to reestablish, offering hope for a safer and more effe...
Researchers have identified a serotonin receptor, HTR7, as a key mediator of eczema and other forms of itch. The study suggests that targeting this receptor may lead to the development of powerful new therapies for chronic itch conditions.
Researchers at the Buck Institute discovered that macrophage-like hemocytes play a crucial role in regulating stem cell activity in the fly gut. This complex signaling interaction helps control intestinal regeneration after damage, but goes awry with age, potentially contributing to human diseases like IBS and colorectal cancer.
Researchers at the Buck Institute have confirmed that Parkinson's disease mutations alter mitochondrial function in human cells for the first time. The study provides a tool for testing potential therapeutics and promises to address concerns about genetic differences between patients.
Researchers at the Buck Institute discovered how rapamycin inhibits mTORC2, a complex linked to metabolic side effects. The study suggests that manipulating FK506 binding proteins could selectively target mTORC1, reducing side effects and improving longevity outcomes.
A study in C. elegans found that excess iron promotes aging by causing dysfunction and malfolding of proteins implicated in the aging process. Treating worms with a metal chelator slowed age-related accumulation of iron, extending lifespan and healthspan.
A study published in PLoS Genetics found that ibuprofen extended the lifespan of yeast, worms, and fruit flies, with treated organisms living up to 15% longer. The research suggests that ibuprofen impacts a process not yet implicated in aging, offering a new approach to studying and understanding the aging process.
Researchers at the Buck Institute discovered that senescent cells secrete PDGF-AA, which accelerates wound closure and heals wounds normally. This finding suggests that cellular senescence may play a beneficial role in human health throughout the lifespan.
Leading scientists have developed a research strategy to expand Geroscience research, focusing on integrating 'pillars of aging' into chronic disease research. The goal is to extend lifespan and healthspan, while offsetting the economic burdens of an aging population with multiple chronic diseases.
Researchers analyzed over 3500 tumors using multiple genomic platforms, revealing that cancers are more likely to be molecularly and genetically similar based on their cell type. The study proposes a new classification system that could lead to personalized cancer treatment and eligibility for novel therapeutics.
A large-scale protein interaction network for Huntington's disease has been identified, providing valuable insights into the disease's pathology. The network implicates the RhoGTPase signaling pathway, which affects cell motility, membrane dynamics, and cell attachment, offering potential therapeutic targets.
A study published in Cell found that altering the symbiotic relationship between bacteria and intestinal cells can promote health and increase lifespan in flies. The research highlights the importance of maintaining a balanced gut microbiome and suggests that this may be key to enjoying a long healthy life.
Research in C. elegans reveals a synergistic five-fold extension of longevity through combined mutations in insulin signaling and the nutrient pathway. This finding suggests the potential for combination therapies to combat aging and age-related diseases.
Researchers have identified widespread regulation of proteins involved in metabolism by the mitochondrial sirtuin, SIRT5. This study found that SIRT5 selectively removes specific sites of succinyl modifications in over 140 different proteins, leading to disruptions in metabolic pathways.
Researchers at the Buck Institute identified a suite of epigenetic markers that separated younger from older individuals, with changes associated to genes regulating neuromuscular junction activity. The study provides a method for studying sarcopenia and offers potential targets for intervention.
Researchers at the Buck Institute discovered a link between ApoE4 and SirT1, an anti-aging protein targeted by resveratrol. Increasing SirT1 may prevent Alzheimer's disease-related abnormalities in brain samples from patients with ApoE4 and AD.
Scientists at the Buck Institute for Research on Aging have identified a mechanism that helps fruit flies adapt to diet changes as young animals, but this mechanism gets misregulated with age, leading to metabolic homeostasis disruption. The study's findings could lead to new treatments that preserve healthy metabolism during aging.
Researchers at the Buck Institute manipulated a signaling pathway implicated in Barrett's esophagus, suggesting a change in stem cell function as the cause of this transformation. This discovery may lead to new targets for therapies and inform the development of more effective treatments for Barrett's esophagus.
Researchers found that rapamycin improved cardiac function and reduced inflammation in aged mice, slowing down heart dysfunction. The study suggests potential benefits for humans with heart disease, as it is already FDA-approved for other indications.
Researchers used RNA interference technology to identify hundreds of molecular targets linked to HD toxicity, including RRAS signaling as a pathologic feature. The study provides a roadmap for discovering new therapies and offers hope for treating the devastating disease.
Researchers at the Buck Institute for Research on Aging found that rapamycin improved function and extended survival in mice with a genetic mutation leading to dilated cardiomyopathy and rare muscular dystrophies. The study suggests a therapeutic possibility for human patients suffering from this form of disease.
A study at the Buck Institute found that fruit flies on dietary restriction need physical activity to reap benefits, whereas humans using caloric restriction may also need sufficient calorie intake. The research suggests a potential target for mimicking diet-restricted lifespan benefits through drug development.
Researchers at the Buck Institute have corrected the genetic mutation responsible for Huntington's Disease using human induced pluripotent stem cells. The corrected cells generated normal neurons in a mouse model of the disease, offering new hope for cell therapy treatments.
Researchers at the Buck Institute have found that modifying scar tissue can potentially improve outcomes in chronic stroke. The study builds on spinal cord injury research and shows that treatments like chondroitinase ABC and glypican can reduce scar tissue size, stimulate neuron growth, and increase survival.
A study published in Science Translational Medicine found that massage reduces inflammation and promotes the growth of new mitochondria in skeletal muscle after intense exercise. The research provides evidence that massage could be a valuable treatment option for individuals with chronic inflammatory diseases or musculoskeletal injuries.
Scientists at Buck Institute discover that inhibiting an mRNA translation factor increases stress response genes and extends lifespan in C. elegans. The study highlights the importance of mRNA translation in aging and may lead to the development of therapeutics to slow age-related diseases.
Researchers at Buck Institute discover lithium profoundly prevents brain damage associated with Parkinson's disease in a mouse model. The study's findings suggest that lithium could be an effective treatment for PD patients at subclinical levels, avoiding side effects.
A new study at the Buck Institute for Research on Aging identifies N-acylethanolamines (NAEs) as a novel metabolic signaling pathway that coordinates the aging response to nutrient availability. This discovery suggests a link between endocannabinoids, dietary restriction, and aging that may be conserved across species.
A study published in Nature reveals that Basic Yellow 1, a neurodegenerative marker, also has anti-aging properties in nematode worms. The compound extends lifespan by more than 50% and slows disease-like pathology in healthy worms.
Douglas Rosenberg invests $3.5 million with Buck Institute to develop treatments for Alzheimer's disease based on small molecule screenings that show promise. The goal is to raise $10 million to get the new drug candidates into early clinical trials.
Researchers at the Buck Institute discovered that insulin signaling affects cell survival and metabolism through translation. The study found that lower insulin signaling is associated with increased tolerance to stress, suggesting a new avenue for disease intervention.
Researchers at the Buck Institute have used human induced pluripotent stem cells (iPSCs) to treat rodent models of Parkinson's Disease, paving the way for potential cell therapies. The study shows that iPSC-derived dopamine-producing neurons can engraft and ameliorate behavioral deficits in animals with PD.
Scientists at the Buck Institute for Research on Aging have discovered a family of enzymes involved in the breakdown of toxic fragments that lead to Huntington's disease. Inhibiting these enzymes, known as matrix metalloproteinases (MMPs), has been shown to reduce the accumulation of toxic fragments associated with HD.
A study in fruit flies reveals a molecular pathway involved in dietary choices, which has implications for humans sharing the same pathway. The research opens doors to developing treatments for metabolic disorders by addressing nutritional imbalances.
A study at the Buck Institute for Age Research found that drugs promoting neurogenesis can lessen the severity of stroke and improve function in rodents. The researchers suggest these drugs, including antidepressants and mood stabilizers, may be suitable for human clinical trials to explore their potential benefits.
A new study using bioinformatics predicts the molecular cause of many inherited genetic diseases by analyzing tens of thousands of mutations. The research led to the creation of a web-based tool available to academic researchers.
A low protein diet boosts mitochondrial function, extending lifespan in flies. This discovery has implications for human aging and diseases such as obesity, diabetes, and cancer.
Cells experiencing DNA damage send signals to neighboring cells, triggering an inflammatory response that can lead to cancer and accelerated aging. The discovery provides a new target for preventing these processes.
Researchers at Buck Institute find HIF-1 protein plays key role in pathway extending lifespan by dietary restriction. Under-expressing HIF-1 leads to increased lifespan even with nutrient-rich diet.
Scientists have discovered a new therapeutic target for Alzheimer's disease by uncovering the normal function of a brain protein. The discovery suggests that the disease stems from an imbalance in signaling between neurons, rather than toxicity from amyloid plaques.
Scientists have discovered biomarkers predicting chronological and physiological age in nematode worms, with implications for human anti-aging therapies. The study's findings, published in Aging Cell, suggest that examining biomarkers over time can provide a scientific baseline for clinical trials.
A Buck Institute study found that lithium increases lifespan in nematode worms by reducing the activity of a gene that modulates chromosome structure. The research highlights the potential for using C. elegans as a model organism to study drug toxicity and genetic impacts of compounds.