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Blockage of EGFR signaling may lead to reversing Alzheimer’s-Like Memory Loss

Blockage of EGFR signaling may lead to reversing Alzheimer’s-Like Memory Loss

In an article entitled, “Epidermal growth factor
receptor” (EGFR)  is a preferred target for treating amyloid-β–induced memory loss”, published online in September 27, 2012, issue of PNAS 1-6, the lead author Lei Wang with eight other associates from seven research groups suggested that a class of presently used anti-cancer drugs as well as several formerly unchecked synthetic compounds show effectiveness in reversing memory loss of Alzheimer’s disease. Alzheimer’s disease is caused by an accumulation of amyloid-β (Aβ) plaques on the brain that induce progressive memory loss. Studies related to Aβ metabolism and toxicity have yielded a wide range of potential drug targets for treating the disease. The team employed two independent research approaches (synaptic plasticity based analysis and behavioral screening of synthetic compounds) to determine if some of these targets are better suited for drug development than others. According to the authors, two clinically available drugs and three synthetic compounds were found to produce positive effects in behavioral tests and antagonize the Aβ oligomers-induced activation of epidermal growth factor receptor (EGFR), a signaling pathway that the authors subsequently linked to Alzheimer’s dementia. These convergent results from parallel approaches, combined with trials with Aβ-induced deficits in transgenic animals, have led the authors conclude that EGFR is a preferred target for treating Aβ-induced memory loss. Apparently, the findings suggest that EGFR inhibition may represent an important therapeutic target for treatment of Alzheimer’s disease in humans. [summarized by Samsad Razzaque – a graduate student of DMB, DU)

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