Molecular therapy for Stroke: A therapeutic mix encompassing docosahexaenoic acid (DHA) and aspirin (ASA) [DHAASA] attenuates hippocampal neurons injury, augments regenerative neurogenesis after Ischemic Stroke, and ameliorates stroke damage and neurological deficits via up regulation of its target genes BDNF and NAMPT, 7/November/2017, 11.43 pm

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Introduction: What they say

A recent study from Research Center for Neurobiology and Department of Neurobiology, Xuzhou Medical College, 209 Tongshan Road, Xuzhou, Jiangsu 221004, PR China; and School of Public Health, Xuzhou Medical College, PR China shows that “HO-1 attenuates hippocampal neurons injury via the activation of BDNF-TrkB-PI3K/Akt signaling pathway in stroke. This study was published, in the July 2  2014 issue of the journal Brain Research,  by Prof  Dong, Qi, and others.

Another study from the Department of Pharmacology, Second Military Medical University, Shanghai, China; Department of Science and Education, Shandong Provincial Hospital affiliated to Shandong University, Jinan, China; and Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China (C.-Y.M.) shows that “Regenerative Neurogenesis After Ischemic Stroke Promoted by Nicotinamide Phosphoribosyltransferase-Nicotinamide Adenine Dinucleotide Cascade” This study was published, in the June 9 2015 issue of the journal Stroke,  by Prof  Miao CY, Zhao Y, and others.


What we say:

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Stroke: A therapeutic mix encompassing docosahexaenoic acid (DHA) and aspirin (ASA) [DHAASA] attenuates hippocampal neurons injury, augments regenerative neurogenesis after Ischemic Stroke, and ameliorates stroke damage and neurological deficits via up regulation of its target genes BDNF and NAMPT

price-200


From research findings to therapeutic opportunity: 

This study suggests that a therapeutic mix encompassing docosahexaenoic acid (DHA) and aspirin (ASA) [DHAASA], by increasing the expression of of its target genes, it may: (1) increase the expression of BDNF and NAMPT (Nicotinamide Phosphoribosyltransferase-Nicotinamide Adenine Dinucleotide); (2) augment neuronal–BDNF-TrkB-PI3K/Akt–survival pathway; (3) increase Sirtuins expression; (4) enhance neural stem cells; (5) promote neural functional recovery; (6) attenuate cerebral /Ischemia reperfusion injury; (7) inhibit neuronal apoptosis; (8) improve learning and memory; and (9) attenuate neurological deficits (Figs.1-2).  [easy_payment currency=”USD”] 

Figure 1. Mechanistic insights into how docosahexaenoic acid (DHA) and aspirin (ASA) protects against stroke. Vildagliptin protects against stroke via up regulation of its target gene BDNF (Brain-derived growth factor) and NAMPT

Together, this study suggests that docosahexaenoic acid (DHA) and aspirin (ASA) [DHAASA] may alleviate stroke, and other neurodegenerative diseases (such as multiple sclerosis, cerebral ataxia etc.), promote brain repair, and extend the lifespan of an individual. Thus, pharmacological formulations encompassing “docosahexaenoic acid (DHA) and aspirin (ASA)  or their analogues, either alone or in combination with other drugs”, may be used to treat stroke and other neurological deficits. 


Details of the idea posted: 

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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

Amount: $200#

Undisclosed mechanistic information: How a therapeutic mix encompassing docosahexaenoic acid (DHA) and aspirin (ASA) [DHAASA] increases the expression of BDNF and NAMPT and attenuates stroke

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

# Research cooperation


References: 

Citation: Boominathan, L., Molecular therapy for Stroke: A therapeutic mix encompassing docosahexaenoic acid (DHA) and aspirin (ASA) [DHAASA] attenuates hippocampal neurons injury, augments regenerative neurogenesis after Ischemic Stroke, and ameliorates stroke damage and neurological deficits via up regulation of its target genes BDNF and NAMPT, 7/November/2017, 11.43 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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