Molecular therapy for stroke: XBP-1 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, 28/November/2018, 12.33 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: XBP-1 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

 


From research findings to therapeutic opportunity: 

XBP-1, by increasing the expression 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 XBP-1 protects against stroke. Relaxin  protects against stroke via upregulation of its target gene BDNF (Brain-derived growth factor) and NAMPT

Figure 2. XBP-1 prevents stroke through induction of Brain-derived growth factor (BDNF) and NAMPT

Together, this study suggests that compounds that induce XBP-1 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, compounds that XBP-1, 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 by Dr L Boominathan Ph.D.

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

Amount: $500#

Undisclosed mechanistic information: How does XBP-1 increase the expression of BDNF and NAMPT?

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

# Research cooperation


References:  

Citation: Boominathan, L., Molecular therapy for stroke: XBP-1 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, 28/November/2018, 12.32 pm,  Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org

Courtesy: When you cite drop us a line at info@genomediscovery.org

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

 

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