Extracorporeal Shock wave therapy for ageing-associated diseases: Extracorporeal Shock wave therapy increases NMN/NAD levels, decreases interaction of DBC1 with PARP1, increases PARP1 activity, promotes DNA repair, augments tolerance against radiation, cancer and aging via down regulation of its target gene, 22/June/2017, 11.30 pm

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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:  Extracorporeal Shock wave therapy for ageing-associated diseases: Extracorporeal Shock wave therapy increases NMN/NAD levels, decreases interaction of DBC1 with PARP1, increases PARP1 activity, promotes DNA repair, augments tolerance against radiation, cancer and aging via down regulation of its target gene

Price 500[easy_payment currency=”USD”]


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, for the first time, an Extracorporeal Shock wave-based therapy for age-associated diseases.

Extracorporeal Shock wave therapy, by increasing 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.

Together, this study suggests, for the first time, how Extracorporeal Shock wave therapy may function as an adjuvant therapy to (1) suppress age-associated overall physiological decline; and (2) improve health/life span.

Given the mechanistic basis of Extracorporeal Shock wave therapy (fig.1), physicians may consider adapting Extracorporeal Shock wave therapy, to prevent age-associated overall physiological decline and improve health/life span.

Figure1. Extracorporeal Shock wave therapy, by increasing NAD+ levels, may suppress ageing-associated overall physiological decline, ageing-associated diseases and improve health/life span

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Details of the research findings: 

Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Undisclosed mechanistic information: How Extracorporeal Shock wave therapy  increases the levels of NMN/NAD to inhibit interaction between DBC1 and PARP1 and to promote DNA repair activity

Amount: $500#

* Research cooperation

For purchase and payment details, you may reach us at info@genomediscovery.org


References:

Citation: Boominathan, L., Extracorporeal Shock wave therapy for ageing-associated diseases: Extracorporeal Shock wave therapy increases NMN/NAD levels, decreases interaction of DBC1 with PARP1, increases PARP1 activity, promotes DNA repair, augments tolerance against radiation, cancer and aging via down regulation of its target gene, 22/June/2017, 11.30 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Web: http://genomediscovery.org or http://newbioideas.com

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