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The results of this study showed that the Korean version of the BDI is appropriate for screening for depression and 16 is the optimal cut-off score for the Korean elderly. Screening of elderly depression with BDI in the community would be valuable when comparing with younger adults and with their former BDI data which were taken when they were young.

Although purinergic compounds are widely involved in the intra-and intercellular communication of the nervous system, little is known of their involvement in the growth and regeneration of neuronal connections. In dissociated cultures, the addition of adenosine or guanosine in the low micromolar range induced goldfish retinal ganglion cells to extend lengthy neurites and express the growth-associated protein GAP-43. These effects were highly specific and did not reflect conversion of the nucleosides to their nucleotide derivatives; pyrimidines, purine nucleotides, and membrane-permeable, nonhydrolyzable cyclic nucleotide analogs were all inactive. The activity of adenosine required its conversion to inosine, because inhibitors of adenosine deaminase rendered adenosine inactive. Exogenously applied inosine and guanosine act directly upon an intracellular target, which may coincide with a kinase described in PC12 cells. In support of this, the effects of the purine nucleosides were blocked with purine transport inhibitors and were inhibited competitively with the purine analog 6-thioguanine (6-TG). In PC12 cells, others have shown that 6-TG blocks nerve growth factor-induced neurite outgrowth and selectively inhibits the activity of protein kinase N, a partially characterized, nerve growth factor-inducible serine-threonine kinase. In both goldfish and rat retinal ganglion cells, 6-TG completely blocked outgrowth induced by other growth factors, and this inhibition was reversed with inosine. These results suggest that axon outgrowth in central nervous system neurons critically involves an intracellular purine-sensitive mechanism.Under normal circumstances, neurons in the adult mammalian central nervous system fail to regenerate axons injured by stroke or trauma, resulting in long lasting disabilities in sensory, motor, or cognitive functions. However, many central nervous system neurons have the potential to regrow their axons if exposed to appropriate growth factors and/or if inhibitory influences that normally prevail in the mature central nervous system are suppressed (1-3). To identify factors that foster axonal regrowth in the central nervous system, we have turned to the classic model of optic nerve regeneration in lower vertebrates. Following injury to the optic nerve, retinal ganglion cells (RGCs) 1 in fish and amphibia re-extend axons that synapse upon appropriate central targets within 1-2 months (4). In a dissociated cell culture model of this system, two factors secreted by optic nerve glia were found to be responsible for inducing axon outgrowth from goldfish RGCs (5, 6). The more potent of these, axogenesis factor-1 (AF-1), has a molecular mass Ͻ1 kDa and stimulates lengthy axonal outgrowth without altering cell survival. AF-2 is a larger polypeptide that exerts a significant but less pronounced effect than AF-1. The specificity of these effects is demonstrated by the inactivity of a host of polypeptide growth factors or low molecular mass differentiation factors in this system (5).In the present st...

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