A recent study from the Department of Psychiatry and Psychotherapy, Georg-August-University Goettingen, Goettingen, Germany shows that “Reducing HDAC6 ameliorates cognitive deficits in a mouse model for Alzheimer’s disease.” This study was published in the 5 Jan’13 issue of the journal EMBO Mol Medicine.
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Small molecule-based therapy for Alzheimer’s disease: NF-κBp65 ameliorates cognitive deficits in Alzheimer’s disease patients via up regulation of its target gene
Given that: (1) in 2006, 26.6 million people worldwide’re afflicted by Alzheimer’s disease; (2) the number of cases diagnosed with Alzheimer’s disease may increase from 26.6 million people in 2006 to 106.4 million in 2050 worldwide; (3) Alzheimer’s disease is the forth leading cause of death in US in the elderly; (4) Alzheimer’s disease is the third most costly disease to treat only after cancer and coronary heart disease; and (5) US$80–100 billion spent in US in caring for patients diagnosed with Alzheimer’s disease, there is an urgent need to find: (i) a cheaper alternative to the existing expensive drugs; and (ii) a side-effect-free natural product-based drug.
This study suggests, for the first time, that NF-κBp65, by increasing the expression of its target gene, it may decrease the expression of HDAC6. Thereby, it may ameliorate cognitive deficits in Alzheimer’s disease patients. Thus, pharmacological formulations encompassing “NF-κBp65 activators” may be used to improve cognitive deficits in Alzheimer’s disease patients.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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To cite: Boominathan, Small molecule-based therapy for Alzheimer’s disease: NF-κBp65 ameliorates cognitive deficits in Alzheimer’s disease patients via up regulation of its target gene, 8/June/2014, 7.56 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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Undisclosed information: How NF-κBp65 decreases HDAC6 expression