Restoration of Cognitive Function with CDK5 Inhibitors en
Researchers in Prof. Richard Tsien’s laboratory have discovered that CDK5 inhibitors could potentially be used for recovery of cognitive function following stroke, traumatic brain injury or neuro-degeneration of afferent inputs. This technology is based on the finding that certain neurons in slices of rat hippocampus which were chronically deprived of activity also had a significant increase in CDK5 (cyclin-dependent kinase 5). Furthermore, application of a known CDK5 inhibitor completely rescued both neural connectivity and synaptic strength in these regions. Because the hippocampus is very important for memory formation and learning, CDK5 inhibitors may help to restore cognitive function by enhancing neural circuits following injury or neurodegeneration in that region. Stage of Research Initial studies of rat hippocampal slices have shown that direct application of roscovitine (a known CDK5 inhibitor) could revert the function of neuron pairs that had been silenced from activity deprivation. [ - ]
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- Restoration of Cognitive Function with CDK5 Inhibitors
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- Researchers in Prof. Richard Tsien’s laboratory have discovered that CDK5 inhibitors could potentially be used for recovery of cognitive function following stroke, traumatic brain injury or neuro-degeneration of afferent inputs. This technology is based on the finding that certain neurons in slices of rat hippocampus which were chronically deprived of activity also had a significant increase in CDK5 (cyclin-dependent kinase 5). Furthermore, application of a known CDK5 inhibitor completely rescued both neural connectivity and synaptic strength in these regions. Because the hippocampus is very important for memory formation and learning, CDK5 inhibitors may help to restore cognitive function by enhancing neural circuits following injury or neurodegeneration in that region. Stage of Research Initial studies of rat hippocampal slices have shown that direct application of roscovitine (a known CDK5 inhibitor) could revert the function of neuron pairs that had been silenced from activity deprivation.
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