As Methuselah Foundation funding grows, thanks to our many generous donors and rising profile, our Strategies for Engineered Negligible Senescence (SENS) research programs will expand beyond the presently active LysoSENS and MitoSENS projects. All SENS research seeks to develop biotechnologies that repair, prevent or make irrelevant the biochemical and cellular damage that causes age-related degeneration – here’s a look at what we have in the pipeline:
AmyloSENS – cleaning up extracellular junk:
The Methuselah Foundation is presently in discussion with leading researchers in this field with a view to initiating work on a vaccine – similar to that developed by Elan for Alzheimer’s disease – to stimulate the aged body to clear the widespread amyloids (particular of transthyretin) responsible for senile systemic amyloidosis.
ApoptoSENS – removing senescent and other “gone bad” cells:
During 2008, the Methuselah Foundation will launch a project to develop a procedure for clearing aged T cells from the blood of mice, and potentially thereafter in primates. This work will be supervised by one of the top professors in the immunosenescence field.
GlycoSENS – breaking down crosslinks and AGEs:
The Methuselah Foundation is currently planning out a project to engineer enzymes capable of cleaving the ubiquitous glucosepane crosslinks, which may comprise as much as 98% of all the long-lived crosslinks in aged human tissue. This work is still in the early planning stages, but we hope to be able to begin full-time research before the end of 2008.
OncoSENS – alter cells to prevent cancer:
The Methuselah Foundation is planning to launch three projects in the OncoSENS strand during 2008.
The first project aims to characterise the enzyme responsible for [alternative lengthening of telomeres], which is still unknown. Recently, however, observations in two different organs have given good reason to consider a hitherto unsuspected gene. A relatively simple series of experiments could test this hypothesis.
The second project addresses a potential problem with the WILT strategy. It’s possible that telomerase activity per se – independent of telomere length – may have roles in maintaining the health of the stem cells themselves, or of their rarely-dividing neighbours in the so-called “stem cell niche”. We are arranging a project to address this question, in the blood of mice, with the world’s leading professor in the area.
Finally, the theory that non-cancer-causing mutations are unlikely to be harmful in a normal lifetime – protagonistic pleiotropy – is not yet widely accepted. We are therefore initiating a rigorous study into the effects of such mutations in mouse brains.