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Question of the Month #8: Aging Damage and Early Early Detection

Posted by Michael Rae on February 12, 2015 | Chief Science Officer's Team

Question of the Month #8: Aging Damage and Early Early Detection. Part of Michael Rae's regular column from the Foundation's newsletter. Q: "Because the cellular and molecular damage of aging is a by-product of metabolism, I have always assumed that it accumulates throughout our entire lives – from when we are a baby until we die. Is this true? Is there any research showing that very young children have low levels of tissue-stiffening crosslinks, extracellular aggregates like beta-amyloid, or intracellular aggregates (like lipofuscin or the ones driving atherosclerosis) in their tissues?"

Bold Leaps Forward for α-Synuclein Immunotherapy

Posted by Michael Rae on December 12, 2014 | Chief Science Officer's Team

α-synuclein (AS) neuropathology is one of the key forms of aging damage driving Parkinson's disease (PD) and aspects of the "normal" loss of cognitive and autonomic nervous control with age. Immunotherapy targeting the clearance of AS aggregates from aging neurons is a key rejuvenation biotechnology for the prevention and reversal of brain aging and PD. The first human clinical trial of an AS-clearing active vaccine in early-stage PD patients was initiated in the summer of 2013. The highly promising results of this first trial have now been announced, and have led to a followup study and the launch of an EU consortium to test it for additional AS-related indications. Contemporaneously, two human trials have been initiated using a second AS-clearing rejuvenation immunotherapy, this one using infused monoclonal antibodies as a passive immunotherapic rather than an antigen-based vaccine. We review progress in this area and its links to the wider progress in PD-related rejuvenation biotechnology.

Rejuvenation Biotechnology: Toward the Indefinite Postponement of Menopause

Posted by Michael Rae on October 08, 2014 | Menopause

A recent interview with SENS Research Foundation Chief Science Officer Dr. Aubrey De Grey evoked an eruption of worldwide media coverage, because of a brief comment he made to the effect that rejuvenation biotechnology could eliminate menopause within twenty years. This post gives some examples of foreseeable biotechnologies carrying us toward that eventuality.

The Neuroprotector's Dilemma: A Potential Neuroprotective Agent with a Janus Face

Posted by Michael Rae on October 01, 2014 | Chief Science Officer's Team

Rejuvenation of the aging brain will require the integrated application of several core rejuvenation biotechnologies, including notably those that remove intra- and extraneuronal aggregates implicated in neurodegenerative aging and mature cell therapy. Numerous aggregate-clearing rejuvenation biotechnologies are now in human trials, whereas mature cell therapy for the brain is a more challenging goal and will not be available for some time. In this context, an alternative approach to maintaining the viability of aging neurons could complement aggregate-clearing therapies to preserve neurons until neural replacement and reinforcement matures. In this post we explore the potential of one recently-emerged approach: inhibition of the unfolded protein response (UPR).

2013 Research Report (Part 7 of 12): Extracellular Aggregates

Posted by Iain Inkster on January 06, 2014 | SRF Research

University of Texas, Houston TX, and Brigham and Women’s Hospital, Harvard University, Boston MA Researchers: Sudhir Paul, Yasuhiro Nishiyama, Stephanie Planque (University of Texas); Brian O’Nuallain (Brigham and Women's Hospital, Harvard Medical School)

2013 Research Report (part 6 of 12): Epimutations

Posted by Iain Inkster on December 05, 2013 | SRF Research

Albert Einstein College of Medicine (AECOM), Bronx NY Researchers: Jan Vijg, Silvia Gravina

2013 Research Report (Part 5 of 12): Lysosomal Aggregates

Posted by Iain Inkster on November 08, 2013 | SRF Research

Researchers: Pedro Alvarez, Jacques Mathieu, Jason Gaspar

2013 Research Report (part 4 of 12): Extracellular Matrix Stiffening

Posted by Iain Inkster on November 01, 2013 | SRF Research

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...

2013 Research Report (part 3 of 12): Cancerous Cells

Posted by Iain Inkster on October 18, 2013 | SRF Research

Researchers: Haroldo Silva, David Halvorsen, Kelsey Moody, Thomas Hunt

2013 Research Report (part 2 of 12): Mitochondrial Mutations

Posted by Iain Inkster on October 09, 2013 | SRF Research

Researchers: Matthew O'Connor, Amutha Boominathan, Jayanthi Vengalam

Unbinding the Mummies: Human Testing of Rejuvenation Biotechnology Targeting α-Synuclein Begins

Posted by Michael Rae on October 02, 2013 | Chief Science Officer's Team

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.

2013 Research Report (part 1 of 12): Lysosomal Aggregates

Posted by Iain Inkster on September 01, 2013 | SRF Research

Researchers: Gouri Yogalingam, Ghezal Beliakoff, Ehud Goldin, Maximus Peto