A new hypothesis proposes that women's reproductive resilience is key to understanding longevity, with menopause representing an important inflection point in the loss of reproductive resilience. This framework challenges traditional views on aging and fertility, highlighting the importance of studying women in longevity research.
The APOE2 gene variant is associated with exceptional longevity and reduced Alzheimer's risk. Research reveals that APOE2 helps human neurons maintain genomic integrity and resist cellular senescence, driving neurodegeneration. This study offers a mechanistic answer to the protective mechanism behind APOE2's role in aging.
The APOE2 gene variant is linked to exceptional longevity and reduced Alzheimer's risk, thanks to its ability to help human neurons keep their DNA intact and resist cellular senescence. This study reveals a previously underappreciated function of the gene, shifting attention away from its role in cholesterol transport.
Dr. Peter Walter joins Buck Institute as Professor to explore fundamental mechanisms of cell health and translate insights into age-related disease prevention and treatment strategies. His work has had a lasting impact on biology, transforming understanding of cellular health and disease.
Researchers discovered that APOE4 causes bone quality deficits specifically in female mice, through a mechanism invisible to standard imaging. The study reveals an unexpected biological link between Alzheimer's risk and skeletal health, pointing to osteocytes as potential early warning signals for both conditions.
Scientists at Buck Institute for Research on Aging developed an orally administered small molecule that completely prevents calcium oxalate kidney stones, protects against kidney failure, and fully restores normal survival in a mouse model of Primary Hyperoxaluria Type 2. The drug candidate, N-propargylglycine (N-PPG), targets a key en...
Healthspan Horizons links real-world longitudinal data with deep discovery science to create uniquely powerful, long-term datasets revealing what drives human healthspan over time. The platform aims to translate discoveries into clearer guidance on what helps people stay resilient, supporting more years of energy, strength, and indepen...
The THRIVE team is developing a PROSPR Intrinsic Capacity score to predict 20-year health outcomes, using wearable data, blood-based biomarkers, and health surveys. The score aims to enable accessible, scalable monitoring of aging and improve interventions.
Researchers propose a new framework to detect chronic diseases earlier by tracking individual biological changes. Advances in technology and AI enable the analysis of complex patterns from wearable devices and biological samples.
A comprehensive roadmap identifies mouse models that incorporate aging as a central element of Parkinson's disease pathogenesis, fostering cooperation among researchers. The collaboration aims to make it easier for scientists to include aging in their efforts to tackle the incurable neurodegenerative motor disease.
Researchers developed a new tool to track changes in the synaptic proteome over time, correlating changes to synaptic dysregulation and synapse loss. The results suggest that toxic tau oligomers impact postsynaptic structures first, leading to a dynamic cascade of events that contribute to neurodegeneration.
A recent Buck Institute study revealed that spaceflight accelerates aging due to changes in immune cell composition and epigenetic markers. However, researchers also found evidence of intrinsic rejuvenation factors that can counteract these age-accelerating stressors.
A comprehensive guide describes the effects of spaceflight on the immune system, including microgravity, cosmic radiation, and sleep disruptions. The study provides integrated mechanistic insights into how these stressors alter immune physiology, with potential relevance in aging research.
Researchers found that a combination of nicotinamide, a-lipoic acid, thiamine, pyridoxamine and piperine reduced AGEs, sticky plaque-like molecules, to curb hunger, lower insulin resistance and extend lifespan in mice. The compounds also reversed some molecular hallmarks of hypothalamic aging.
Researchers found that a high fiber diet reduced Alzheimer's-related frailty and tremor in mice by restoring balance in the gut immune system. This discovery provides a potential new therapeutic pathway for the disease.
Girls who go through puberty before age 11 have double the risk of type 2 diabetes, heart failure, and obesity, while women who give birth before 21 have quadruple the risk. Later puberty and childbirth are associated with longer lifespan, lower frailty, and reduced disease risk.
The Buck Institute is pioneering a cloud-based platform to simulate the dynamic behavior of microbial cells, overcoming current whole-cell models' limitations. The SIMBA project aims to advance our understanding of bacterial behavior and address critical challenges in biomanufacturing and national security.
A new study from the Buck Institute has uncovered how breaking down glycogen in neurons may protect against toxic protein buildup and degeneration. Researchers found that restoring an enzyme called glycogen phosphorylase can reduce tau-related damage and improve oxidative stress reduction.
A proof-of-concept study shows that chimeric antigen receptors (CARs) can distinguish between tau tangles and various forms of toxic amyloid plaques, two key contributors to Alzheimer's disease pathology. The technology has the potential to deliver therapeutic drugs directly to affected areas of the brain with reduced side effects.
A new biological age 'clock' measures intrinsic capacity, sum of six key functions determining healthy aging. The IC Clock uses DNA methylation in blood to assess functional decline and links to healthier lifestyle choices.
A first-of-its-kind clinical trial demonstrates the impact of therapeutic plasma exchange on biological age, reducing it by an average of 2.6 years. The study used multi-omics biomarkers to investigate the effects of TPE on biological age and found promising results for its potential in disease prevention and longevity applications.
The Buck Institute's hybrid intervention combines a daily ketone ester with ICOPE-INTENSE, a personalized approach improving Intrinsic Capacity and age-related functions. The team aims to restore muscle, cognition, and immune function by 10 years in one year or less.
The Buck Institute and Phenome Health have been awarded up to $52M by ARPA-H to develop a groundbreaking research project that aims to predict and prevent diseases using advanced analytics and AI. The project, known as PATH, will utilize machine learning and digital wearables to create personalized recommendations for healthy aging.
Researchers at the Buck Institute found that ketone bodies interact directly with misfolded proteins, altering their solubility and structure to be cleared through autophagy. This discovery suggests a new form of metabolic regulation of protein quality control in the brain, with potential therapeutic applications.
Researchers analyzed correlations between fruit fly and human data to identify key metabolites impacting lifespan. Threonine was found to extend lifespan in flies and show promise as a therapeutic target for aging interventions.
A ketogenic diet has been shown to improve memory and healthspan in aging mice by activating a critical signaling pathway. The study found that the main ketone body produced during a ketogenic diet, BHB, plays a crucial role in activating this pathway.
Scientists studied how microgravity impacts human peripheral blood mononuclear cells and identified potential compounds to counter its effects, including the antioxidant quercetin. The findings have implications for immune aging on Earth and provide a resource for developing countermeasures.
Researchers found that boosting mitochondrial health can combat protein clumping linked to both aging and Alzheimer's. The study identifies a core insoluble proteome enriched with numerous proteins not previously considered, offering new targets for exploration.
Researchers at Buck Institute for Research on Aging propose an alternate strategy for reversing memory problems in Alzheimer's disease by targeting the KIBRA protein. The findings suggest that KIBRA can rescue mechanisms that promote synapse resilience, potentially leading to improved memory function.
Researchers have identified the role of OXR1 in maintaining retromer function, which protects neurons from oxidative damage. Boosting this gene's expression may help extend human lifespan. The study provides potential therapeutic targets to slow brain aging and age-related neurodegenerative diseases.
Researchers discovered novel functions for autophagy genes in controlling different forms of cellular disposal, including misfolded proteins. In nematode C. elegans, inhibition of early-acting autophagy genes extended lifespan and reduced protein aggregates, highlighting a new pathway in aging.
The Buck Institute has partnered with Hevolution Foundation to pioneer new scientific initiatives targeting aging. The partnership aims to accelerate discoveries toward therapeutic interventions specifically targeting the aging process, which is linked to age-related chronic diseases.
Researchers at Buck Institute identified a new drug-like molecule that keeps mitochondria healthy via mitophagy, a process that removes and recycles damaged mitochondria. The compound, MIC, extended lifespan in worms and improved mitochondrial function in mouse muscle cells.
Scientists at Buck Institute reveal how NAD+ decline affects female reproductive function and longevity. Adding CD38 to the puzzle, they found that this enzyme degrades NAD+, accelerating aging processes. Targeting CD38 may offer new approaches to enhance fertility and overall healthspan.
Buck Institute researchers discover that advanced glycation end products (AGEs) in processed foods increase hunger and test willpower, contributing to overeating and obesity. By understanding the biochemical signaling pathway behind AGEs, scientists may develop strategies to limit their accumulation and promote healthy eating.
The Buck Institute is leading a clinical trial to determine the effects of ketone ester supplementation on frailty, a condition that develops following age-related decline in multiple physiological systems. The trial aims to recruit 180 people at risk for frailty and will measure muscle strength as its primary outcome.
Researchers at Buck Institute for Research on Aging developed a bioavailable compound that selectively inhibits free radical production in mitochondria, preventing and treating metabolic syndrome in mice. The compound, S1QEL1.719, decreases fat accumulation, improves glucose tolerance, and normalizes fasting insulin levels.
The T32 program has trained 110 fellows in research on aging over the past 25 years, leading to faculty positions, biotech jobs, and scientific publications in top journals. The grant renewal highlights the program's success in increasing human healthspan and its impact on the Bay Area aging community.
Researchers have developed a non-invasive method to track human aging using retinal scans, which are less expensive and more accurate than other aging clocks. The study found that changes in the eye can provide an actionable evaluation of gero-protective therapeutics, offering a new tool for tracking aging.
Research reveals that brain function networks are affected differently by aging, gender, and blood immune factors. The study found correlations between cytokine clock, brain shrinkage, and gender, with females having a faster ticking cytokine clock.
Researchers have designed a smart cell-based delivery system to treat Alzheimer's disease by targeting multiple pathologies, reducing the risk of side effects. The system uses bio-synthesizable drugs and immune cells to deliver combination therapy that addresses all pathologies in a targeted manner.
Buck scientists introduce mechanoimmunology, a new discipline that explores the role of physical forces in immune cell responses. The study reveals that mechanical cues tune immune cell behavior, potentially leading to new treatments for various disorders.
Researchers at Buck Institute discover that blood-brain barrier cells influence neuron function and can cause problems rather than just being protective. This finding opens up new avenues for therapies targeting neurodegenerative diseases like Alzheimer's and Parkinson's.
Buck Institute researchers found that dietary restriction can extend lifespan in fruit flies due to changes in their circadian rhythms, particularly in the eye. The study suggests that the eye plays a role in regulating lifespan, which may have implications for human health and aging.
Researchers discovered that a conserved receptor molecule called Tom70 coordinates the balance between protein production and import into mitochondria. This finding ties to increased lifespan and delayed mitochondrial dysfunction when Tom70 levels are elevated. The study provides new insights into aging and age-related diseases.
Researchers found a common genetic variant that may protect women with endometriosis or polycystic ovary syndrome from future heart disease. The variant also appears to lower the risk of breast and other cancers in women who experience preeclampsia.
Researchers at the Buck Institute discovered a naturally occurring metabolite, 25-hydroxycholesteral, that significantly reduces senescent cells in multiple cell types and improves muscle mass in aged mice. The molecule targets CRYAB, a small heat shock protein associated with age-related diseases like myopathies.
Scientists have mapped the tau interactome, showing that mutant tau impacts mitochondria function in human neurons. The study also reveals a mechanism for tau release from neurons and its binding to mitochondrial proteins, which may inform future studies on preventing diseased tau spread.
Researchers at Buck Institute will identify and characterize senescent cells in human ovaries, breast tissue, and skeletal muscle to better understand their role in age-related diseases. The study aims to develop therapeutics to improve human health by quelling the damaging effects of senescent cells.
The Buck Institute has been awarded a $14.3 million grant from the NIH to study cellular senescence, a hallmark of aging, as a driver of Alzheimer's disease and other age-related dementias. Researchers will investigate new mechanisms that can be developed into interventions to treat patients.