Transient brain ischemia has been shown to induce hyperphosphorylation of the microtu-bule-associated protein tau. To further determine the mechanisms underlying these processes, Dr, Bo Song and co-workers from School of Life Sciences, Tsinghua University in China found for the first time that the interaction of tau with glycogen synthase kinase (GSK)-3β and protein phosphatase 2A is altered during transient brain ischemia. In addition, the researchers found that the neuroprotective function of lithium chloride may depend partly on the altered phosphorylation of tau, by regulating the associations between tau, GSK-3β and protein phosphatase 2A during cerebral ischemia. These findings were published in the Neural Regeneration Research (Vol. 8, No. 34, 2013).
Source: Neural Regeneration Research