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Jo, Sangmee A.,Ahn, Kyungsook,Kim, Eunkyung,Kim, Hwa-Su,Jo, Inho,Kim, Doh Kwan,Han, Changsoo,Park, Moon Ho S. Karger AG 2008 Dementia and geriatric cognitive disorders Vol.25 No.2
<P><I>Background:</I> β-Site amyloid precursor protein cleaving enzyme (BACE) is a candidate risk factor for Alzheimer’s disease (AD) from its key role in β-amyloid generation. Previous genetic association studies of <I>BACE1</I> gene have yielded conflicting results. This study is an attempt to clarify whether the common SNP in exon 5 of <I>BACE1</I> (rs638405, Val262) is associated with a risk for late-onset AD. <I>Methods:</I> We genotyped a synonymous C/G polymorphism of <I>BACE1</I> located in exon 5 and apolipoprotein E (ApoE) in 248 AD patients and 224 healthy persons. A meta-analysis with pooled data from four Chinese studies and our results was performed. <I>Results:</I> The allele and genotype frequencies of <I>BACE1</I> polymorphism were not significantly different between cases and controls (p > 0.05) in the Korean population. A meta-analysis of previously published Asian populations including Koreans showed evidence of a weak association (p = 0.0555 for genotypes, p = 0.0352 for alleles). However, a significant association between the CC genotype and AD was observed in the ApoE-ε4-positive groups (p = 0.0044, OR = 1.995; 95% CI = 1.319-3.018). <I>Conclusion:</I> These data suggest that BACE1 polymorphism in exon 5 influences risk for late-onset AD in those carrying the ApoE ε4 allele.</P><P>Copyright © 2008 S. Karger AG, Basel</P>
Yoo, Chulbae,Ahn, Kyungsook,Park, Jeong Eun,Kim, Min-Ju,Jo, Sangmee Ahn Elsevier 2010 FEBS letters Vol.584 No.19
<P><B>Abstract</B></P><P>The accumulation of beta amyloid (Aβ) has been a primary target for Alzheimer disease therapeutic strategies. Previously, we discovered an activity from <I>Streptomyces</I> sp. KK565 growth media that inhibits Aβ aggregation. The active component was an aminopeptidase and named <I>Streptomyces</I> sp. KK565 aminopeptidase (SKAP). SKAP cleaved N-terminal amino-acids of Aβ<SUB>1–42</SUB> monomer, inhibited formation of fibrils and protected Aβ<SUB>1–42</SUB>-induced neurotoxicity. Over-expression of a human homolog of SKAP, glutamate carboxypeptidase II (hGCPII) in Aβ-oversynthesizing cells dramatically reduced the Aβ levels. These findings suggest a possible role of M28 family peptidases in preventing Aβ deposits in mammalian brain.</P><P><B>Structured summary</B></P><P>MINT-7992796: <I>SKAP</I> (uniprotkb:Q306T3) <I>physically interacts</I> (MI:0915) with <I>Abeta</I> (uniprotkb:P05067) by <I>protease assay</I> (MI:0435)</P><P>MINT-7992752, MINT-7992778: <I>SKAP</I> (uniprotkb:Q306T3) <I>binds</I> (MI:0407) to <I>Abeta</I> (uniprotkb:P05067) by <I>protease assay</I> (MI:0435)</P>
Han, Changsu,Jo, Sangmee Ahn,Seo, Ji A,Kim, Byoung Gwon,Kim, Nan Hee,Jo, Inho,Park, Moon Ho,Park, Kun Woo Elsevier 2009 ARCHIVES OF GERONTOLOGY AND GERIATRICS Vol.49 No.2
<P><B>Abstract</B></P> <P>Obesity has a strong association with cardiovascular and metabolic diseases, which have also been linked with dementia. While recent studies have reported an association between mid-life obesity and dementia, the role that later-life obesity may have is less clear. A total of 721 community-dwelling elderly (60–85 years old) were selected. Obesity parameters, like body mass index (BMI), waist-hip ratio (WHR), waist circumference (WC), and percent body fat (PBF), as well as cognitive functions were measured over a period of approximately 2 years, and then the relationships between these variables were assessed. The change in cognitive function in the elderly was associated with the baseline assessment of BMI (linearly, <I>β</I> =0.092), WC (quadratic, <I>β</I> =1.333), and PBF (linearly, <I>β</I> =0.097). Using multiple regression analyses, the differences exist in the change of cognitive function over time according to the sex. For men, increased obesity over time when obese in the baseline assessment (BMI, WHR, WC) were associated with a positive change in cognitive function. For women, a decreased obesity over time when obese in the baseline assessment (WHR) and an increased obesity over time when they had a normal adiposity in the baseline assessment (WC) were both associated with cognitive decline. The relationship between obesity and cognitive decline in the elderly is complex and some differences exist between the sexes. The application of the “Jolly Fat” hypothesis to cognitive function can only be applied to elderly men and not to elderly women.</P>
Awareness of putative risk factors for Alzheimer’s disease among elderly Koreans
Park, Moon Ho,Jo, Sangmee Ahn,Jo, Inho,Kim, Eunkyung,Woo, Eun Kyung,Kim, Sung-Soo,Eun, Su-Yong,Han, Changsu,Park, Min Kyu Blackwell Publishing Ltd 2008 Acta neuropsychiatrica Vol.20 No.1
<P>Objective</P><P>Although there are rapidly growing concerns about the high rates of cognitive dysfunction in Korea, the knowledge of risk factors for Alzheimer’s disease (AD) among the general public in Korea remains to be elucidated.</P><P>Methods</P><P>A total of 2767 randomly selected subjects from the Ansan Geriatric Study were questioned on their knowledge of putative risk factors for AD. Their answers were compared with their sociodemographic data and other variables.</P><P>Results</P><P>The most common stated risk factor was being older (59.6%), followed by head trauma (33.6%) and cerebrovascular disease (30.4%). However, a substandard education, which is a known risk factor, was considered significant by only 9.5% of the subjects. Predictors for a worse knowledge of the risk factors for AD were being older, a lower level of education, lower economic status and the attitude that dementia is not curable.</P><P>Conclusion</P><P>This study revealed that misunderstanding about AD is more prevalent in older subjects and those with a lower level of education, and so public health education on the basic concepts of AD should be targeted at this population.</P>
Cho, Du-Hyong,Choi, Yoon Jung,Jo, Sangmee Ahn,Ryou, Jungsang,Kim, Jin Yi,Chung, Jongkyeong,Jo, Inho American Physiological Society 2006 American journal of physiology. Cell physiology Vol.291 No.2
<P>Thiazolidinediones (TZDs), synthetic peroxisome proliferator-activated receptor gamma (PPARgamma) ligands, have been implicated in the inhibition of protein synthesis in a variety of cells, but the underlying mechanisms remain obscure. We report that troglitazone, the first TZD drug, acutely inhibited protein synthesis by decreasing p70 S6 kinase (p70S6K) activity in bovine aortic endothelial cells (BAEC). This inhibition was not accompanied by decreased phosphorylation status or in vitro kinase activity of mammalian target of rapamycin (mTOR). Furthermore, cotreatment with rapamycin, a specific mTOR inhibitor, and troglitazone additively inhibited both p70S6K activity and protein synthesis, suggesting that the inhibitory effects of troglitazone are not mediated by mTOR. Overexpression of the wild-type p70S6K gene significantly reversed the troglitazone-induced inhibition of protein synthesis, indicating an important role of p70S6K. Okadaic acid, a protein phosphatase 2A (PP2A) inhibitor, partially reversed the troglitazone-induced inhibition of p70S6K activity and protein synthesis. Although troglitazone did not alter total cellular PP2A activity, it increased the physical association between p70S6K and PP2A, suggesting an underlying molecular mechanism. GW9662, a PPARgamma antagonist, did not alter any of the observed inhibitory effects. Finally, we also found that the mTOR-independent inhibitory mechanism of troglitazone holds for the TZDs ciglitazone, pioglitazone, and rosiglitazone, in BAEC and other types of endothelial cells tested. In conclusion, our data demonstrate for the first time that troglitazone (and perhaps other TZDs) acutely decreases p70S6K activity through a PP2A-dependent mechanism that is independent of mTOR and PPARgamma, leading to the inhibition of protein synthesis in endothelial cells.</P>
Choi, Ji-Young,Ko, Jun-Hyeok,Jo, Sangmee Ahn Elsevier 2018 Biochemical and biophysical research communication Vol.497 No.1
<P><B>Abstract</B></P> <P>Our previous study showed that the level of glutamate carboxypeptidase II (GCPII) protein is regulated by valproic acid, a histone deacetylase (HDAC) inhibitor, through acetylation of lysine residue in the GCPII protein in human astrocytes, U-87MG. The present study further investigated which HDAC subtype is involved in the acetylation of GCPII. The results revealed that GCPII interacted with HDAC1 but not with HDAC2, HDAC3, HDAC4, HDAC5, and HDAC6. Overexpression of catalytic domain (1–56 aa)-deleted HDAC1, which poorly binds to GCPII, enhanced lysine acetylation in GCPII and increased the level of GCPII protein when compared with that of the wild-type HDAC1. Further experiments showed that HDAC1 regulated the stability of GCPII protein. These data suggest that acetylation of GCPII is facilitated by HDAC1, and the acetylated GCPII is more stable than the non-acetylated GCPII. Additional experiments using siRNA HDAC1 and by <I>HDAC1</I> overexpression confirmed the role of HDAC1 in regulating the stability of GCPII protein. Further, database search of acetylation and ubiquitination sites showed four candidate lysine sites in human GCPII protein that can be both acetylated and ubiquitinylated (K207, K479, K491, and K699). Mutation (lysine residues to arginine (R)) analysis showed that in the presence of cycloheximide K479R- and K491R-hGCPII mutants were less ubiquitinylated and degraded, and decrease in the level of GCPII protein by HDAC1 was significantly blocked by K479R mutants. These data suggest that K479 is a possible site of acetylation or ubiquitination. Furthermore, the results also demonstrate that the stability of GCPII protein is regulated by HDAC1 through acetylation at the lysine 479 residue.</P> <P><B>Highlights</B></P> <P> <UL> <LI> GCPII interacts specifically with HDAC1 which is present in the non-nuclear fraction. </LI> <LI> HDAC1 regulates the stability of GCPII protein. </LI> <LI> Mutation at lysine sites in human GCPII (K479R and K491R) reduces the ubiquitination. </LI> <LI> Mutation at 479 lysine residue of human GCPII blocks HDAC1-mediated decrease in the level of GCPII protein. </LI> </UL> </P>
( Yea-hyun Leem ),( Sang-sun Yoon ),( Sangmee Ahn Jo ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.3
Previous studies have shown disrupted synaptic plasticity and neural activity in depression. Such alteration is strongly associated with disrupted synaptic structures. Chronic stress has been known to induce changes in dendritic structure in the basolateral amygdala (BLA) and medial prefrontal cortex (mPFC), but antidepressant effect on structure of these brain areas has been unclear. Here, the effects of imipramine on dendritic spine density and morphology in BLA and mPFC subregions of stressed mice were examined. Chronic restraint stress caused depressive-like behaviors such as enhanced social avoidance and despair level coincident with differential changes in dendritic spine structure. Chronic stress enhanced dendritic spine density in the lateral nucleus of BLA with no significant change in the basal nucleus of BLA, and altered the proportion of stubby or mushroom spines in both subregions. Conversely, in the apical and basal mPFC, chronic stress caused a significant reduction in spine density. The proportion of stubby or mushroom spines in these subregions overall reduced while the proportion of thin spines increased after repeated stress. Interestingly, most of these structural alterations by chronic stress were reversed by imipramine. In addition, structural changes caused by stress and blocking the changes by imipramine were corelated well with altered activation and expression of synaptic plasticity-promoting molecules such as phospho-CREB, phospho-CAMKII, and PSD-95. Collectively, our data suggest that imipramine modulates stress-induced changes in synaptic structure and synaptic plasticity-promoting molecules in a coordinated manner although structural and molecular alterations induced by stress are distinct in the BLA and mPFC.