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A08-T006




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Basic Information:

Title:	Optimized Human Performance: Mitochondrial Energetics
Program:	STTR
Technology Area:	Human Systems
Open Date:	2/19/2008
Close Date:	3/19/2008

Description:

The modern Army is constrained by biology. Highly qualified and very experienced soldiers routinely leave the Army because they are old; their physical and/or cognitive performance capabilities are significantly less than that of a 20 year old. The biological basis of this reduction in performance capability may be an injury, but in most cases is simply due to the reduced efficiency of old mitochondria, resulting in reduced levels of energy (adenosine triphosphate) provided to the body to power cognitive and physical tasks. The ability to stimulate mitochondrial energy production would extend the time that soldiers remain fit for duty, boost soldier physical and performance capabilities, and expand the age range of suitable recruits. It would also eliminate the current dichotomy of the ideal soldier being optimized both for youth (high performance capabilities) and experience. The past twenty years have seen a revolutionary breakthrough in understanding how mitochondria function. Human mitochondria are a network of approximately 2,000 proteins, exquisitely integrated into a larger network of approximately 100,000 cellular proteins, and again functionally integrated into a larger network of 3 billion cells. All of the corresponding genes have been cloned and sequenced. The biochemical basis of oxidative phosphorylation is well understood and genetic polymorphisms leading to altered energetics and performance capabilities are well documented. The scientific understanding and the technology to undertake high throughput screening to identify compounds that affect mitochondria is now possible.

Objective:

Develop metabolic supplements to optimize adenosine triphosphate production in eukaryotes.

Phase I:

Design, construct, and demonstrate proof of concept function for a high throughput assay to screen for compounds that increase mitochondrial copy number and/or the efficiency of mitochondrial oxidative phosphorylation. Identify libraries of compounds that will be tested in phase II. Establish a methodology for follow-up characterization of active compounds.

Phase II:

Screen libraries of compounds for stimulatory effects on mitochondrial copy number and mitochondrial oxidative phosphorylation. Characterize active compounds using genetics, genomics, bioinformatics, and biochemical approaches.

Commercialization Potential:

The world contains approximately 4.2 billion people over the age of twenty. Even a small enhancement of cognitive capacity in these individuals would probably have an impact on the world economy rivaling that of the internet. The commercial market for a compound that could reverse the effects of aging on human energetics would be more than significant. The cost of Social Security in the U.S. is expected to approach 7% of the gross domestic product (GDP); reducing this cost by any significant degree would also have substantial impact on federal obligations and expenditures.

References:

1. Balaban, R.S. Nemoto, S., and Finkel, T. 2005. Mitochondria, oxidants, and aging. Cell 120(4):483-95. 2. Beal, M.F. 2005. Mitochondria take center stage in aging and neurodegeneration. Ann Neurol 58(4):495-505. 3. Huang, H. and Manton, K.G. 2004. The role of oxidative damage in mitochondria during aging. Front Biosci 9:1100-17. 4. Lee, H.C. and Wei, Y.H. 1997. Role of mitochondria in human aging. J Biomed Sci 4(6):319-26. 5. Lenaz, G., Bovina, C., DAurelio, M., Fato, R., Formiggini, G., Genova, M.L., Giuliano, G., Merlopich, M., Paolucci, U., Castelli, G., and Ventura B. 2002. Role of mitochondria in oxidative stress and aging. Ann N Y Acad Sci 959:199-213. 6. Linford, N.J., Schriner, S.E., and Robinovitch, P.S. 2006. Oxidative damage and aging: spotlight on mitochondria. Cancer Res 1:66(5):2497-9. 7. Navarro, A., and Boveris, A. 2004. Rat brain and liver mitochondria develop oxidative stress and lose enzymatic activities on aging. Am J. Physiol Regul Integr Comp Physiol 287(5):1244-9.

STTR Keywords

mitochondria, oxidative phosphorylation

TechMatch Keyword(s):

Human Systems

Biomedical technology

Human Performance

Medical Science, Medicine, and Biology

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