Bioassay for monitoring the anti-aging effect of cord blood treatment

Abstract

Background: Treating aged animals with plasma of an early developmental stage (e.g, umbilical cord plasma) showed an impressive potential to slow age-associated degradation of neuronal and cognitive functions. Translating such findings to clinical realities, however, requires effective ways for assessing treatment efficacy; ideal methods should be minimally invasive, amenable for serial assays, cost-effective, and quantitative.Methods: We developed a new biosensor approach to monitor anti-aging therapy. We advanced two key sensor components: i) a blood-borne metabolite was identified as a surrogate aging-marker; and ii) a compact and cost-effective assay system was developed for on-site applications. We treated aged mice either with human umbilical cord plasma or saline; unbiased metabolite profiling on mouse plasma revealed arachidonic acid (AA) as a potent indicator associated with anti-aging effect. We next implemented a competitive magneto-electrochemical sensor (cMES) optimized for AA detection directly from plasma. The developed platform could detect AA directly from small volumes of plasma (0.5 µL) within 1.5 hour.Results: cMES assays confirmed a strong correlation between AA levels and anti-aging effect: AA levels, while decreasing with aging, increased in the plasma-treated aged mice which also showed improved learning and memory performance.Conclusions: The cMES platform will empower both pre- and clinical anti-aging research by enabling minimally invasive, longitudinal treatment surveillance; these capacities will accelerate the development of anti-aging therapies, improving the quality of individual lives.

Mitochondria–plasma membrane interactions and communication

“…Interestingly, it has been shown that stress is the main elicitor of TNTs (hyperglycemia, acidified medium, endotoxin, serum starvation, H 2 O 2 , cytokines), similar to some of the mitochondria–PM interactions described above ( 14 , 15 , 61 ). Although the molecular mechanisms are still poorly understood, Miro1 and p53 have been involved, and importantly, Cx43 has been found critical for electric coupling and mitochondria transfer in a model of lung disease ( 65 , 66 ), or after oxygen/glucose deprivation ( 67 ).…”