Research Projects

  • To restore youthful function to cells failing in many age-related diseases, we need to purge them of stubborn wastes that accumulate during biological aging. At Rice University, SENS Foundation is funding research to identify, test, and improve the function of natural enzymes in the environment capable of degrading specific wastes, so that we can harness them to give the same ability into our cells.

    LysoSENS
  • Along with mutations in our cellular DNA, some cells also suffer "epimutations:" permanent damage to the structures that control the expression of the underlying genes. SENS Foundation has identified biomedical strategies to keep the body healthy and functioning normally despite the low level of mutations that accumulate with age; the same strategies will also work for epimutations, if their rate of accumulation is similarly low. To give the first assurance that the rate of epimutation-hampered cell accumulation over the adult lifespan is low enough for the strategy to be comprehensive, SENS Foundation is funding research at Albert Einstein College of Medicine to put new methods to use in determining that rate more definitively.

    OncoSENS
  • Immune cell function declines with age, as the thymus loses the cells that "educate" the precursors of immune cells called killer T-cells, and as defective killer T-cells accumulate and suppress the full diversity of youthful, functional killer Ts that target newly-encountered threats. At the  University of Arizona, SENS Foundation is funding research to restore the production of new killer T-cells while making room for them by purging the defective cells from the system.

    ApoptoSENS
  • Along with mutations in our chromosomes, aging bodies also accumulate disabling "deletion" mutations in the separate DNA housed in the energy-producing mitochondria. SENS Foundation has identified the placement of functioning "backup copies" of mitochondrial genes in the cell nucleus as an "engineering" solution to preempt the metabolic mayhem these mutations ultimately create. The Foundation is now funding the expansion of work in the lab of Dr. Marisol Corral-Debrinski at the Institut de la Vision at Pierre and Marie Curie University, Paris, who has developed the most promising method to achieve this goal for most, if not all, of the relevant mitochondrial genes.

    MitoSENS
  • Aging bodies slowly accumulate extracellular aggregates around their cells: sticky clumps of proteins that interfere with cells and tissues carrying out their function.  Two such proteins are responsible for age-related disorders in heart function: the "cardiac amyloidoses", senile systemic amyloidosis (SSA) and isolated atrial amyloidosis (IAA). Removing these aggregates is necessary to rejuvenate the structure and function of the aging heart. SENS Foundation is funding work by Drs. Sudhir Paul at the University of Texas-Houston Medical School and Brian O’Nuallain at University College Dublin to develop antibodies that would target the identification and catalytic breakdown of these aggregates, letting aging hearts beat with the freedom of youth.

    AmyloSENS
  • Senescence is a genetic program which normal dividing cells invoke in order to prevent excessive cellular growth. This is initially a protective mechanism, preventing cells undergoing stresses such as DNA damage from becoming cancerous, and keeping the wound-healing response from overstepping its bounds and generating an overgrowth of fibrous connective tissue.

    ApoptoSENS