The need for disease-modifying therapies in Alzheimer's disease, and the strength of the case for aggregated beta-amyloid as a target, have recently driven substantial regulatory reform and innovations in clinical trial design to open up the path for faster and more effective human testing and approval of novel Alzheimer's therapeutics. The first fruits of these changes are a series of large, late-stage clinical trials of immunotherapies targeting the removal of beta-amyloid from the brain. These reforms and precedents open up the path for human testing and approval of future rejuvenation biotechnologies.
We all know that mitochondria are the cell's "powerhouse" for energy. One interesting fact about these organelles is that they have their own DNA in addition to the nuclear DNA that we are all aware of. However, the mitochondrial DNA is prone to mutations due to constant exposure from reactive oxygen species because it is not encased in a nuclear envelope nor does it have efficient repair mechanisms to correct mutations as they occur. Amutha Boominathan explains how moving the mitochondrial genes to the nucleus, where it's safer to express them for function, would let mitochondria keep producing energy normally, even after mitochondrial mutations have occurred.
Jayanthi Vengalam explains her work with the Mitochondrial Mutation team, with consequences for acute diseases such as diabetes, Parkinson's and Alzheimer's
Haroldo Silva explains why he joined OncoSENS team at the SRF Research Center and explains the role of telomere lengthening in cancer.
Engineering of new thymus tissue is a key rejuvenation biotechnology, to prevent or reverse the dramatic rise in morbidity and mortality from infectious disease that begins in the seventh decade of life. SENS Research Foundation is supporting thymus engineering research at the Wake Forest Institute of Regenerative medicine. In an important first, researchers at UCSF have derived a simple thymus-like tissue transplant that gave promising signs of restoring the ability to help form mature T-cells.
Dr. Ehud Goldin has recently joined SENS Research Foundation as head of the Research Center’s A2E degradation project. His work will be to enable the lysosomes of retinal pigment epithelial cells to degrade A2E...
Two quarter-century long studies on the effects of Calorie restriction in nonhuman primates have come to opposing results. What do these results mean for the human translatability of CR, and the future of therapies to prevent and cure the diseases and disabilities of aging?
Cell Reprogramming Leaps Ahead: First Transplant of Primate Induced Pluripotent Cell-Derived Neurons into Donor BrainPosted by Michael Rae on April 17, 2013 | Chief Science Officer's Team
"Reprogramming" of adult differentiated cells into pluripotent stem cells is an exciting method in biology that holds enormous promise for rejuvenation biotechnology. Now, for the first time, Dr. Su-Chun Zhang and coworkers at the University of Wisconsin-Madison have successfully generated neurons from reprogrammed nonhuman primate cells, transplanted them back into the same animal's brain, and seen them successfully and cleanly integrate into the local tissue.
David Brindley, a SENS Research Foundation-funded PhD candidate at the University of Oxford, is the lead author on a new publication in the journal BioProcess International discussing the automation of cell therapy biomanufacturing.
SENS Research Foundation is delighted to welcome Dr. George Church, Professor of Genetics at Harvard Medical School, to our Research Advisory Board. Our RAB plays a key role in our mission to change the way the world researches and treats age-related disease. By applying expertise from multiple relevant areas, the Board assures that efforts and resources are directed along the most promising avenues.
SENS Research Foundation has established a new research center at Cambridge University and a collaboration with scientists at Yale University. The mission: develop new therapies to repair a critical form of molecular damage that drives the slow stiffening of the arteries with age. Such rejuvenation biotechnologies could prevent such deadly and disabling diseases of aging as stroke and kidney disease.
The preliminary results of a clinical trial for a disease of "premature aging" - Hutchinson-Gilford Progeria Syndrome (HGPS) - are hopeful and inspiring. However, they cannot directly inform the development of rejuvenation biotechnologies; although the symptoms of HGPS are similar to those observed in aging, there is no evidence to suggest that the underlying mechanism is pathologically significant in those not afflicted with the disease.