Introduction: What they say
A study from Department of Genetics, Paul F. Glenn Center for the Biology of Aging, Harvard Medical School, Boston, MA, USA; and Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, New South Wales 2052, Australia shows that “A conserved NAD+ binding pocket that regulates protein-protein interactions during aging.” This research paper was published, in the 24 March 2017 issue of the journal “Science“ [One of the best research journals in Science with an I.F of 34+], by Prof. David A. Sinclair, Jun Li, and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Probiotic-based therapy for aging-associated diseases and Lifespan extension: A therapeutic mix encompassing Probiotic Bifidobacterium LKM512 and Arginine inhibits the interaction of DBC1 with PARP1, increases the PARP1 activity, promotes DNA repair, augments tolerance against radiation, cancer, and aging, via down-regulation of its target gene
What is known?
Prof. David A. Sinclair’s research team has recently shown that: (a) increased levels of NAD+ (found in non-aged tissues) inhibits the interaction the between DBC1 (deleted in breast cancer 1) and PARP1 [poly(adenosine diphosphate–ribose) polymerase]; and promotes DNA repair; (b) decreased levels of NAD+ (found in aged tissues) promotes the interaction between DBC1 and PARP1 and inhibits DNA repair; (c) aged cells/tissues that are low in NAD+ are radiation-sensitive, cancer-prone and prone to accelerated ageing; and (d) ageing-associated diseases can be reversed by increasing the concentration of NAD+ in ageing tissues, suggesting that ageing-associated diseases, in part, can be reversed by NAD+ supplementation in older animals.
From research findings to therapeutic opportunity:
This study suggests a Probiotic-based therapy for both ageing-associated diseases and life-span extension. A therapeutic mix encompassing Probiotic Bifidobacterium LKM512 and Arginine (ABLKM512), by decreasing the expression of its target gene, it may increase the levels of NAMPT and NMN/NAD+. Thereby, it may: (1) increase plasma NMN levels and tissue NAD+ availability; (2) inhibit the interaction between DBC1 and PARP1; (3) augment PARP1’s DNA repair activity; (4) protect against radiation; (5) protect against cancer; and (6) prevent age-associated gene expression pattern and accelerated ageing.
Figure 1. A therapeutic mix encompassing Probiotic Bifidobacterium LKM512 and Arginine (ABLKM512) functions an anti-aging and a longevity-promoting agent. ABLKM512, by increasing NAD+ levels, may suppress ageing-associated overall physiological decline, ageing-associated diseases and improve health/lifespan
Figure 2. A therapeutic mix encompassing Probiotic Bifidobacterium LKM512 and Arginine (ABLKM512) promotes health/lifespan by increasing the levels of NAD+.
Figure 3. While restoring NAD+ levels attenuate ageing features and promote DNA repair activity, a pharmaceutical mix encompassing Probiotic Bifidobacterium LKM512 and Arginine (ABLKM512) may promote health/lifespan by increasing the levels of NAD+
Thus, pharmacological formulations encompassing “Probiotic Bifidobacterium LKM512 and Arginine (ABLKM512), either alone or in combination with other compounds,” may be used to suppress age-associated overall physiological decline and improve health/lifespan.
Details of the research findings:
Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.
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Undisclosed mechanistic information: How does a therapeutic mix encompassing Probiotic Bifidobacterium LKM512 and Arginine (ABLKM512) increase the levels of NMN/NAD?
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References:
Citation: Boominathan, L., Probiotic-based therapy for aging-associated diseases and Lifespan extension: A therapeutic mix encompassing Probiotic Bifidobacterium LKM512 and Arginine inhibits the interaction of DBC1 with PARP1, increases the PARP1 activity, promotes DNA repair, augments tolerance against radiation, cancer, and aging, via down-regulation of its target gene, 23/July/2019, 8.03 am, Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org
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