Albert Einstein College of Medicine (AECOM), Bronx NY Researchers: Jan Vijg, Silvia Gravina
Researchers: Pedro Alvarez, Jacques Mathieu, Jason Gaspar
Our arteries slowly stiffen with age, in substantial part because of chemical crosslinking of their structural proteins by blood sugar and other fuels in the circulation. Like the crosslinking that causes rubber windshield wipers to become stiff and brittle over time, the crosslinking of arterial proteins with age leaves us with increasingly rigid blood vessels...
Researchers: Haroldo Silva, David Halvorsen, Kelsey Moody, Thomas Hunt
Researchers: Matthew O'Connor, Amutha Boominathan, Jayanthi Vengalam
Aggregates of the neuronal membrane protein α-synuclein accumulate in the aging brain and are implicated in the non-motor symptoms of Parkinson's disease and related disorders, as well as subtler age-related dysfunction of the autonomic and peripheral nervous system. Preclinical evidence demonstrates that immunotherapeutic clearance of these aggregates in transgenic animals rescues Parkinson's-like behavioral and cognitive dysfunction. With support from a major Parkinson's research and advocacy charity, an Austrian biotech firm has advanced a first-in-class rejuvenation biotechnology targeting α-synuclein aggregates into Phase I clinical trials.
Researchers: Gouri Yogalingam, Ghezal Beliakoff, Ehud Goldin, Maximus Peto
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.