Cyclin-dependent kinase-5 (CDK5) is predominantly active in the nervous system and it is well established that CDK5 is essential in neuronal development. In addition to its recognized role in development, there is increasing evidence that CDK5 may be involved in the pathogenesis of several neurodegenerative disorders. Although studies have shown that CDK5 can modulate cell death and survival, controversy still exists as to the exact role CDK5 may play in neurodegenerative processes. This review will highlight recent data on the possible roles of CDK5 in neurodegeneration.
A refined battery of neurological tests, SNAP (Simple Neuroassessment of Asymmetric Impairment), was developed and validated to efficiently assess neurological deficits induced in a mouse model of traumatic brain injury. Four to 7-month old mice were subjected to unilateral controlled cortical impact or sham injury (craniectomy only). Several behavioral tests (SNAP, beam walk, foot fault, and water maze) were used to assess functional deficits. SNAP was unique among these in that it required no expensive equipment and was performed in less than 5 min per mouse. SNAP demonstrated a high level of sensitivity and specificity as determined by receiver-operator characteristics curve analysis. Interrater reliability was good, as determined by Cohen's Kappa method and by comparing the sensitivity and specificity across various raters. SNAP detected deficits in proprioception, visual fields, and motor strength in brain-injured mice at 3 days, and was sensitive enough to detect magnitude and recovery of injury. The contribution of individual battery components changed as a function of time after injury, however, each was important to the overall SNAP score. SNAP provided a sensitive, reliable, time-efficient and cost-effective means of assessing neurological deficits in mice after unilateral brain injury.
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