Part of: AmyloSENS ApoptoSENS GlycoSENS LysoSENS MitoSENS OncoSENS RepleniSENS This project has recently concluded; further information will be published in the near future. Applied StemCell, Inc. Principal Investigator: Dr. Ruby Yanru Chen-Tsai The CRISPR/Cas9 gene editing system has the ability to make precisely-targeted changes in the genetic sequence – a clear strength of the platform …
When blood from a biologically aged animal is transfused into a young one, the young animal suffers “pro-aging” effects. By contrast, reducing the burden of “pro-aging” signaling factors in old blood is not enough to remove existing damage from a similar-aged mouse’s biologically aged tissues.
A comprehensive suite of rejuvenation biotechnologies must include the removal of extracellular aggregates from aging cells and tissues, particularly the brain. Recent work indicates that up-regulation of the activity of the native lysosomal pathway for clearance of beta-amyloid (Abeta) by the small molecule PADK can reverse existing Alzheimer-like pathology in mouse models, although caution is required in interpreting these results in the context of human disease.
Neurofibrillary tangles – accumulations of abnormal tau protein – are thought to play a central role in Alzheimer’s disease and other neurodegenerative conditions. Here we review a recent report in which immunotherapy was used to clear tau aggregates from a highly accurate mouse tauopathy model, resulting in functional recovery on multiple cognitive tests.
Much of the distraction in the literature of biogerontology, and an even higher ratio of studies cited and promoted in the popular media and the dietary supplement industry, derives from methodologically-poor lifespan studies in mice (or occasionally rats). In these studies, an increase in mean or maximal lifespan is reported, relative to short-lived controls, and claimed to be informative about the universal, degenerative aging process and the prospects for extending healthy life in humans living in the developed world.
Unlike mouse embryonic stem cells (ESCs), human ESCs are highly prone to death after enzymatic dissociation from a growing cell cluster; as a result, researchers are forced to rely on far more laborious methods for their expansion. New research at the Scripps Institute has revealed the molecular basis for this frustrating limitation, and also uncovered two small-molecule drugs able to greatly improve the cells’ survival.
In conversation with Adam Ford, Dr. Aubrey de Grey explains how recent extraordinary results with senolytic drugs suggest that the milestone of “Robust Mouse Rejuvenation” – a key step towards comprehensively undoing human aging – could be as little as three years away.
We’re hiring a full-time Research Assistant (RA) to join our small but dynamic Senescence Immunology group, for a project investigating the mechanisms involved in the age-dependent decline in immune surveillance of senescent cells in cell culture and mouse models.
A model organism is a non-human species that can be studied to understand particular biological phenomena. Some common examples of model organisms are the microscopic nematode C. elegans, the fruit fly Drosophila melanogaster, and the mouse. They serve as good substitutes when it isn’t possible or practical to study humans directly.
Aging laboratory rodents are the foundation of our ability to study the degenerative aging process, and develop the rejuvenation biotechnologies that will arrest and reverse it. They’re also expensive, logistically intensive, and in short supply. A new UK initiative has been establish to greatly expand what we can learn from the aging animals in our collective care, and to get a fuller picture of aging and its deceleration and reversal than has hitherto been possible.
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