Novato, CA, United States

Buck Institute for Age Research

thebuck.org
Novato, CA, United States

The Buck Institute for Research on Aging is the United States' first independent biomedical research institute devoted solely to research on aging and age-related disease. The mission of the Buck Institute is to extend the healthspan, the healthy years of life.The Institute, a nonprofit organization located in Novato, California, began its research program in 1999. It is named for Marin County philanthropists Leonard and Beryl Hamilton Buck, whose estate funded the generous endowment that helped establish the Institute, and the Buck Trust currently contributes approximately $6 million annually to support the Institute's work. In May 2007, the Institute established a cooperative agreement with the University of California's Davis and Merced campuses to coordinate stem-cell research, a move hailed by UC as a collaboration that "strengthens California's leadership in stem cell research and moves it forward in an efficient, safe and cost-effective manner."The campus of the Buck Institute was designed by architect I. M. Pei, who submitted an unsolicited proposal to design the research facility. Wikipedia.

SEARCH FILTERS
Time filter
Source Type

Campisi J.,Buck Institute for Age Research | Campisi J.,Lawrence Berkeley National Laboratory
Current Opinion in Genetics and Development | Year: 2011

Cellular senescence arrests the proliferation of potential cancer cells, and so is a potent tumor suppressive mechanism, akin to apoptosis. Or is it? Why did cells evolve an anti-cancer mechanism that arrests, rather than kills, would-be tumor cells? Recent discoveries that senescent cells secrete growth factors, proteases and cytokines provide a shifting view-from senescence as a cell autonomous suppressor of tumorigenesis to senescence as a means to mobilize the systemic and local tissue milieu for repair. In some instances, this mobilization benefits the organism, but in others it can be detrimental. These discoveries provide potential mechanisms by which cellular senescence might contribute to the diverse, and seemingly incongruent, processes of tumor suppression, tumor promotion, tissue repair, and aging. © 2010 Elsevier Ltd.


Burtner C.R.,University of Washington | Kennedy B.K.,University of Washington | Kennedy B.K.,Buck Institute for Age Research | Kennedy B.K.,Guangdong Medical College
Nature Reviews Molecular Cell Biology | Year: 2010

One of the many debated topics in ageing research is whether progeroid syndromes are really accelerated forms of human ageing. The answer requires a better understanding of the normal ageing process and the molecular pathology underlying these rare diseases. Exciting recent findings regarding a severe human progeria, Hutchinsonĝ€"Gilford progeria syndrome, have implicated molecular changes that are also linked to normal ageing, such as genome instability, telomere attrition, premature senescence and defective stem cell homeostasis in disease development. These observations, coupled with genetic studies of longevity, lead to a hypothesis whereby progeria syndromes accelerate a subset of the pathological changes that together drive the normal ageing process. © 2010 Macmillan Publishers Limited. All rights reserved.


Brand M.D.,Buck Institute for Age Research
Experimental Gerontology | Year: 2010

Mitochondrial superoxide production is an important source of reactive oxygen species in cells, and may cause or contribute to ageing and the diseases of ageing. Seven major sites of superoxide production in mammalian mitochondria are known and widely accepted. In descending order of maximum capacity they are the ubiquinone-binding sites in complex I (site IQ) and complex III (site IIIQo), glycerol 3-phosphate dehydrogenase, the flavin in complex I (site IF), the electron transferring flavoprotein:Q oxidoreductase (ETFQOR) of fatty acid beta-oxidation, and pyruvate and 2-oxoglutarate dehydrogenases. None of these sites is fully characterized and for some we only have sketchy information. The topology of the sites is important because it determines whether or not a site will produce superoxide in the mitochondrial matrix and be able to damage mitochondrial DNA. All sites produce superoxide in the matrix; site IIIQo and glycerol 3-phosphate dehydrogenase also produce superoxide to the intermembrane space. The relative contribution of each site to mitochondrial reactive oxygen species generation in the absence of electron transport inhibitors is unknown in isolated mitochondria, in cells or in vivo, and may vary considerably with species, tissue, substrate, energy demand and oxygen tension. © 2010 Elsevier Inc.


Azzu V.,MRC Mitochondrial Biology Unit | Brand M.D.,MRC Mitochondrial Biology Unit | Brand M.D.,Buck Institute for Age Research
Trends in Biochemical Sciences | Year: 2010

Mitochondrial uncoupling proteins disengage substrate oxidation from ADP phosphorylation by dissipating the proton electrochemical gradient that is required for ATP synthesis. In doing this, the archetypal uncoupling protein, UCP1, mediates adaptive thermogenesis. By contrast, its paralogues UCP2 and UCP3 are not thought to mediate whole body thermogenesis in mammals. Instead, they have been implicated in a variety of physiological and pathological processes, including protection from oxidative stress, negative regulation of glucose sensing systems and the adaptation of fatty acid oxidation capacity to starving. Although much work has been devoted to how these proteins are activated, little is known of the mechanisms that reverse this activation. © 2009 Elsevier Ltd.


Katewa S.D.,Buck Institute for Age Research | Kapahi P.,Buck Institute for Age Research
Experimental Gerontology | Year: 2011

Extensive studies in model organisms in the last few decades have revealed that aging is subject to profound genetic influence. The conserved nutrient sensing TOR (Target of Rapamycin) pathway is emerging as a key regulator of lifespan and healthspan in various species from yeast to mammals. The TOR signaling pathway plays a critical role in determining how a eukaryotic cell or a cellular system co-ordinates its growth, development and aging in response to constant changes in its surrounding environment? TOR integrates signals originating from changes in growth factors, nutrient availability, energy status and various physiological stresses. Each of these inputs is specialized to sense particular signal(s), and conveys it to the TOR complex which in turn relays the signal to downstream outputs to appropriately respond to the environmental changes. These outputs include mRNA translation, autophagy, transcription, metabolism, cell survival, proliferation and growth amongst a number of other cellular processes, some of which influence organismal lifespan. Here we review the contribution of the model organism Drosophila in the understanding of TOR signaling and the various biological processes it modulates that may impact on aging. Drosophila was the first organism where the nutrient dependent effects of the TOR pathway on lifespan were first uncovered. We also discuss how the nutrient-sensing TOR pathway appears to be critically important for mediating the longevity effects of dietary restriction (DR), a potent environmental method of lifespan extension by nutrient limitation. Identifying the molecular mechanisms that modulate lifespan downstream of TOR is being intensely investigated and there is hope that these are likely to serve as potential targets for amelioration of age-related diseases and enhance healthful lifespan extension in humans. © 2010 Elsevier Inc.


Katewa S.D.,Buck Institute for Age Research | Kapahi P.,Buck Institute for Age Research
Aging Cell | Year: 2010

Dietary restriction (DR) is a robust nongenetic, nonpharmacological intervention that is known to increase active and healthy lifespan in a variety of species. Despite a variety of differences in the protocols and the way DR is carried out in different species, conserved relationships are emerging among multiple species. 2009 saw the field of DR mature with important mechanistic insights from multiple species. A report of lifespan extension in rapamycin-treated mice suggested that the TOR pathway, a conserved mediator of DR in invertebrates, may also be critical to DR effects in mammals. 2009 also saw exciting discoveries related to DR in various organisms including yeast, worms, flies, mice, monkeys and humans. These studies complement each other and together aim to deliver the promise of postponing aging and age-related diseases by revealing the underlying mechanisms of the protective effects of DR. Here, we summarize a few of the reports published in 2009 that we believe provide novel directions and an improved understanding of dietary restriction. © 2010 The Authors Journal compilation © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2010.


Patent
Buck Institute for Age Research | Date: 2015-07-15

The invention generally relates to the prevention and/or treatment of cancer, and, more specifically, to the treatment of tumors, including solid tumors and their metastases, without radiation or standard chemotherapeutic agents. In one embodiment, the invention involves a method comprising: a) providing a subject with tumor cells, b) removing at least a portion of said tumor cells from said subject to create removed cells, c) treating at least a portion of said removed cells ex vivo, using stimulating agents, including thapsigargin and/or thapsigargin-related compounds, so as to create treated tumor cells; and d) introducing said treated tumor cells (or fragments thereof) in vivo into the same subject to generate anticancer therapeutic effects.


Patent
Buck Institute for Age Research | Date: 2011-08-19

The invention provides compositions and methods for the treatment of mild cognitive impairment (MCI), and for inhibiting, reducing, delaying and/or preventing the progression of MCI to Alzheimers disease. The methods entail administering an effective amount of one or more compounds selected from the group consisting of tropisetron, disulfuram, honokiol and nimetazepam. The methods also are useful for prophylactic and therapeutic treatment of amyloidogenic diseases, including Alzheimers disease.


Patent
Buck Institute for Age Research | Date: 2016-01-20

The invention generally relates to the prevention and/or treatment of cancer, and, more specifically, to the treatment of tumors, including solid tumors and their metastases, without radiation or standard chemotherapeutic agents. In one embodiment, the invention involves a method comprising: a) providing a subject with tumor cells, b) removing at least a portion of said tumor cells from said subject to create removed cells, c) treating at least a portion of said removed cells ex vivo, using stimulating agents, including thapsigargin and/or thapsigargin-related compounds, so as to create treated tumor cells; and d) introducing said treated tumor cells (or fragments thereof) in vivo into the same subject to generate anticancer therapeutic effects.


Patent
Buck Institute for Age Research | Date: 2013-09-04

This invention provides a novel screening system for identifying p53 mimetics/agonists. Also provided are small organic molecules that act as effective p53 mimetics/agonists.

Loading Buck Institute for Age Research collaborators
Loading Buck Institute for Age Research collaborators