Alpha-synuclein aggregates are a key form of aging damage in the brain, linked to a spectrum of symptoms in Parkinson's disease beyond the classic motor symptoms. The first amyloSENS-style immunotherapy to clear this pathology out of the brain was advanced into clinical trials by Austrian biotech firm AFFiRiS AG. Now two more such therapies have entered human testing. Although the trials are in their earliest stages, they bring the hope that this rejuvenation biotechnology will begin preventing and reversing Parkinson's disease and less specific disorders of aging soon.
Question of the Month #15: Would Other Rejuvenation Biotechnologies Keep Us Cancer-Free? Part of Michael Rae's regular column from the Foundation's newsletter.
Question of the Month #13: How Can Thymic Regeneration Combat Age-Related Autoimmunity? Part of Michael Rae's regular column from the Foundation's newsletter.
Question of the Month #12: Energy-Carrying Molecules to Boost Aging Mitochondria? Part of Michael Rae's regular column from the Foundation's newsletter.
Press Release: New Study Funded by SENS Research Foundation Sheds Greater Light on Diabetes and the Aging Process
Question of the Month #11: Are Mitochondrial Mutations Really All That Important? Part of Michael Rae's regular column from the Foundation's newsletter.
Question of the Month #10: Rejuvenation for calcification amelioration? Part of Michael Rae's regular column from the Foundation's newsletter.
Question of the Month #9: What is the role of novel diagnostics in rejuvenation biotechnologies? Part of Michael Rae's regular column from the Foundation's newsletter.
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?"
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.
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.
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).