Policy Analysis for Implementing Neuroethics in Korea’s Brain Research Promotion Act

In 1998, Korea implemented the Brain Research Promotion Act (BRPA), a law to revamp the field of neuroscience at the national level. However, despite numerous revisions including the definition and classification of neuroscience and the national plans for the training and education systems, the governance for neuroethics has not been integrated into the Act. The ethical issues raised by neuroscience and neurotechnology remain unchallenged, especially given the focus on the industrial purpose of the technology. In the current study, we analyzed the BRPA revision process by using Kingdon’s Multiple Streams Framework to determine the problems faced by the process. We propose a new strategy, including neuroethics governance and a national committee, to promote interdisciplinary neuroscience research and strengthen neuroethics in Korea.

The Characteristics of Prostate Cancer with Metabolic Syndrome in Korean Men / 대한비뇨기과학회지

PURPOSE: Metabolic syndrome, a concurrence of disturbed glucose and insulin metabolism, overweight, abdominal fat distribution, dyslipidemia, and hypertension, has been reported to have some association with prostate cancer. Here, we assessed the relationship between metabolic syndrome and prostate cancer. MATERIALS AND METHODS: We assessed a total of 261 men who underwent radical retropubic prostatectomy between January 2004 and May 2005. The patients were stratified into two groups, with metabolic syndrome (n=75) or without (n=186). Metabolic syndrome was defined by the criteria of National Cholesterol Education Program Adult Treatment Panel III. We compared the clinical and pathologic features of specimens between the groups. RESULTS: There was no significant difference between the two groups in terms of mean age, serum prostate specific antigen level, prostate size, Gleason score, and pathologic stage. The tumor volume of prostate cancer was significantly higher in the metabolic syndrome group (6.6+/-5.5cc vs 5.0+/-4.5cc, p=0.010). No significant differences were observed in extracapsular extension, seminal vesicle invasion, bladder neck invasion, angiolymphatic invasion, perineural invasion, and multicentricity of cancer between the two groups. As the component of metabolic syndrome increased, the tumor volume was also found to increase (p-value=0.025). CONCLUSIONS: The data from our study support that metabolic syndrome is closely associated with the development and progression of prostate cancer.

Alzheimer's Disease and Apoptosis

Apoptosis is a form of cell death in which the cells shrink and exhibit nuclear chromatin condensation and DNA fragmentation, and yet maintain membrane integrity. Many lines of evidence have shown that brain neurons are vulnerable to degeneration by apoptosis. Also it has been suggested that apoptosis is one of the mechanism contributing neuronal loss in Alzheimer's disease(AD), since the conditions in the disease(A beta peptide, oxidative stress, low energy metabolism) are the inducers that activate apoptosis. Indeed some neurons in vulnerable regions of the AD brain show DNA damage, chromatin condensation, and apoptic bodies. Consistently, mutations in AD causative genes(Amyloid precursor protein, Presenilin-1 and Presenilin-2) increase A beta peptide1-42(Abeta1-42) and sensitize neuronal cell to apoposis. However, several lines of evidence have shown that the location of neuronal loss and A beta peptide deposition is not correlated in AD brain and transgenic mice brain over-expressing Abeta1-42. Taken together, these data may indicated that A beta peptide(and other causative factors of AD) can interact with other cellular insults or risk factors to exacerbate pathological mechansim of AD through apoptosis. Thus, this review discusses possible role and mechanism of apoptosis in AD.

The Change of Expression in Amyloid Precursor Protein mRNA and Amyloid Precursor Protein by Transient Ischemia

Although the mechanism has not been clearly understood, it has been reported that various altered gene expressions are induced by cerebral ischemia. In order to investigate the effects of transient cerebral ischemia on the amyloid precursor protein(APP) metabolism, the 3 isoforms of APP mRNA and the APP were examined. Rats were given ischemic insult through middle cerebral artery occlusion and reperfusions using blunted 4-0 nylon thread after exposure of cervical region. Groups were assigned with each being 1 hour occlusion and 1hr, 3hrs, 8hrs, 1day, 3days, 7days after reperfusion. The rats were then sacrificed and cerebral cortex of each animal was dissected. The mRNA level of APP770, 751, 695 was investigated by reverse transcription coupled polymerase chain reaction (RT-PCR) and the protein amount of APP was investigated by Western blotting method. The results showed that transient ischemia induced the change of APP mRNA. The APP mRNA which encodes the KPI(Kunitz-type protease inhibitor) domain began to increase after 1 day, reaching a maximun at 3 days, and then decreased to control level in the 7 days. The protein level of APP was same until 7 days. We conclude that transient cerebral ischemia alters the gene expression of APP isoforms. Therefore, we speculate that some factors regulating the splicing of APP gene transcript may also undergo ischemia-induced changes and the increase in levels of KPI-APP following ischemia might be associated with pathological changes during the ischemic process.

Effect of Immobilization Stress on the Expression of Amyloid Precursor Protein in the Mouse Brain

BACKGROUND: The Central nervous system(CNS) plays a essential role in mediating~stress responses. However, the enact mechanism of the CNS in mediating stress responses has not been clarified sufficiently as yet. Stress may cause brain dysfunction including cognitive dysfunction which was most commonly found in Alzheimer's dementia. Amyloid precursor protein(APP) is a large, ubiquitously distributed and evolutionarily conserved molecule whose function remains unknown. Although the precise function of APP following injury to the CNS such as stab and kainic acid lesion. However, there have not been reports on the effects of stress on the expression of amyloid precursor protein in the brain. This study was undertaken to elucidate the effects of stress on the expression of APP in the mouse brain. METHODS: The several brain region was isolated from the mouse that was in the immoblization stress for 30 min, 1 hour, and 2 hours. The mouse brain was divided into 5 regions, cerebral cortex, cerebellum hippocampus, midbrain and thalamus, corpus striatum and brain stem. The change of mRNA was examined in the several brain regions using Northern blot hybridization. RESULTS: The amounts of APP mRNA in the cerebral cortex, hippocampus and brain stem were found to be significantly increased after stress for 30 minutes and to 1.each a maximum after stress for 1 hour and to normal range at stress for 2 hours. On the contray, the contents of APP mRNA in midbrain and thalamus were decreased after stress for 30 minutes and sustained after stress for 2 hours. CONCLUSION: These findings suggest that APP may not be static but functional protein reactive to stress and stress may increase the levels of APP mRNA especially in Alzheimer disease associated sites such as cerebral cortex and hippocampus, which may contriute to the pathogenesis of Alzheimer disease.