Rescuing the cerebral ischemia-mediated brain damage: TGF-β attenuates cerebral ischemia-mediated brain damage via down regulation of its target gene, 13/June/2015, 11.29 pm

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A recent study from the Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, IL, USA shows that “Post-transcriptional inactivation of matrix metalloproteinase-12 after focal cerebral ischemia attenuates brain damage.” This study was published in the 8 May 2015 issue of the Journal “Sci Reports” by Prof Veeravalli KK, Chelluboina B and Others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMDreports that: Rescuing the cerebral ischemia-mediated brain damage: TGF-β attenuates cerebral ischemia-mediated brain damage attenuates cerebral ischemia-mediated brain damage via down regulation of its target gene

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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CitationBoominathan, Rescuing the cerebral ischemia-mediated brain damage: TGF-β attenuates cerebral ischemia-mediated brain damage via down regulation of its target gene, 13/June/2015, 11.29 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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Significance: 

Given that: (1)  stroke is the second leading cause of death worldwide in 2011; (2)  11% of total deaths were due to stroke; (3) stroke deaths increased by 10% in the developing world; (3) south asians account for 40% global stroke deaths; (4) the  economic cost spent in europe27 countries for the treatment of stroke was little more than 27 billion euro dollars, while in the united states in 2008 $65.5 billion dollars; and (5) approximately 85% of all stroke deaths are recorded in low- and middle-income countries, there is an urgent need to find:  (i) an effective therapy against stroke; (ii) a cheaper alternative to the existing expensive drugs; and (iii) a side-effect-free natural product-based drug.

This study suggests a molecular therapy for Ischemic Stroke.  TGF-β, by decreasing the expression of its target gene, it may: (1) increase the expression of myelin basic protein; (2) decrease the expression of MMP-9 & TNFα; (3) decrease infarct size; (4) promote neuroprotection; and (5) attenuate cerebral ischemia-mediated brain damage.  Thus, pharmacological formulations encompassing TGF-β activators may be used to treat Ischemic Stroke.

Undisclosed information: How TGF-β attenuates cerebral ischemia-mediated brain damage

* Research cooperation

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