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  <title>ScholarWorks Community:</title>
  <link rel="alternate" href="https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/81" />
  <subtitle />
  <id>https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/81</id>
  <updated>2025-12-30T13:31:53Z</updated>
  <dc:date>2025-12-30T13:31:53Z</dc:date>
  <entry>
    <title>임상연구-검사법-국책</title>
    <link rel="alternate" href="https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/72968" />
    <author>
      <name>노지훈</name>
    </author>
    <id>https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/72968</id>
    <updated>2024-07-31T11:00:41Z</updated>
    <published>2026-12-01T00:00:00Z</published>
    <summary type="text">Title: 임상연구-검사법-국책
Authors: 노지훈</summary>
    <dc:date>2026-12-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Peripheral blood transcriptome signatures indicate environmental influences in monozygotic twins discordant for Alzheimer&amp;apos;s disease</title>
    <link rel="alternate" href="https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78647" />
    <author>
      <name>Roh, Jee Hoon</name>
    </author>
    <author>
      <name>Park, Chanhyeok</name>
    </author>
    <author>
      <name>Kim, Suhyun</name>
    </author>
    <author>
      <name>Shin, Jong-Yeon</name>
    </author>
    <author>
      <name>Kim, Jong-Il</name>
    </author>
    <author>
      <name>Yoon, Young-Wook</name>
    </author>
    <author>
      <name>Park, Kun-Woo</name>
    </author>
    <author>
      <name>Stein, Thor D.</name>
    </author>
    <author>
      <name>Lee, Junghee</name>
    </author>
    <author>
      <name>Lee, Jae-Hong</name>
    </author>
    <author>
      <name>Ryu, Hoon</name>
    </author>
    <id>https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78647</id>
    <updated>2025-11-17T04:30:18Z</updated>
    <published>2026-02-01T00:00:00Z</published>
    <summary type="text">Title: Peripheral blood transcriptome signatures indicate environmental influences in monozygotic twins discordant for Alzheimer&amp;apos;s disease
Authors: Roh, Jee Hoon; Park, Chanhyeok; Kim, Suhyun; Shin, Jong-Yeon; Kim, Jong-Il; Yoon, Young-Wook; Park, Kun-Woo; Stein, Thor D.; Lee, Junghee; Lee, Jae-Hong; Ryu, Hoon
Abstract: Environmental factors have been proposed to contribute to the pathogenesis of Alzheimer&amp;apos;s disease (AD). Because monozygotic (MZ) twins share identical genetic backgrounds, they provide a unique model to disentangle genetic and environmental contributions to disease-related molecular changes. Herein, we investigated MZ twins who lived distinctly different lives and became discordant for AD, and analyzed which transcriptome signatures were altered in the affected twin. We further examined whether these alterations paralleled those found in sporadic AD patients compared with individuals with normal cognition (NC). Whole transcriptome sequencing was performed on mRNAs isolated from peripheral white blood cells of the discordant MZ twins, and the results were compared with transcriptome datasets from blood cells and postmortem brains of sporadic AD patients and NC subjects. In the AD twin, transcripts associated with inflammatory and immune responses were up-regulated, whereas transcripts related to signal recognition particle-mediated protein targeting pathways were down-regulated. Biological network analysis revealed dense connectivity among up-regulated genes linked to cell chemotaxis, cytokine production, and inflammatory response. Heatmap analysis demonstrated differential expression of transcripts related to histone, DNA, and RNA modifications in the AD twin. Comparative analyses with transcriptome data from postmortem brains of sporadic AD patients confirmed similarly up-regulated inflammatory responses in both groups. Taken together, these findings suggest that environmental factors can shape transcriptome signatures related to inflammation and immune pathways, and that such gene expression alterations may ultimately contribute to AD development.</summary>
    <dc:date>2026-02-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Intrinsic excitability changes in amygdala neurons following observational fear conditioning in mice</title>
    <link rel="alternate" href="https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78930" />
    <author>
      <name>Hong, Eun-Hwa</name>
    </author>
    <author>
      <name>Kim, Yang In</name>
    </author>
    <author>
      <name>Kim, Young-Beom</name>
    </author>
    <author>
      <name>Choi, June-Seek</name>
    </author>
    <id>https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78930</id>
    <updated>2025-12-24T06:30:13Z</updated>
    <published>2026-01-01T00:00:00Z</published>
    <summary type="text">Title: Intrinsic excitability changes in amygdala neurons following observational fear conditioning in mice
Authors: Hong, Eun-Hwa; Kim, Yang In; Kim, Young-Beom; Choi, June-Seek
Abstract: Observational fear conditioning (OFC) is used to study the social transmission of aversive information within a social context. In a typical experiment, observers exhibit defensive responses after witnessing a demonstrator&amp;apos;s reaction to repeated footshocks. Despite its relevance to socially acquired fear, the underlying cellular plasticity remain poorly understood. In this study, we investigated changes in the intrinsic excitability of amygdala neurons following OFC. In Experiment 1, we classified amygdala neurons into burst, regular and late-firing types, and found that burst-firing neurons in the basolateral amygdala (BLA) and late-firing neurons in the central amygdala (CeA) of the observer mice showed increased intrinsic neuronal excitability. In Experiment 2, we found that intrinsic excitability changes in both BLA and CeA neurons were selectively enhanced when observers witnessed the demonstrator&amp;apos;s high-frequency jumping behavior, but not freezing. In Experiment 3, an opaque wall and a distractor were used to investigate the role of visual transmission during OFC. Although both the opaque wall and the distractor blocked observer&amp;apos;s fear response, burst-firing BLA neurons in the distractor group nonetheless exhibited enhanced excitability, whereas late-firing CeA neurons did not. These findings suggest that amygdala subpopulations play dissociable roles in OFC: burst-firing BLA neurons appear to be involved in processing emotionally salient sensory cues, while late-firing CeA neurons appear to mediate the expression of socially acquired fear.</summary>
    <dc:date>2026-01-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Cross-Sectional FDG in Down Syndrome and Autosomal Dominant Alzheimer&amp;apos;s Disease</title>
    <link rel="alternate" href="https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78425" />
    <author>
      <name>Abdelmoity, Omar</name>
    </author>
    <author>
      <name>Wisch, Julie K.</name>
    </author>
    <author>
      <name>Kennedy, James T.</name>
    </author>
    <author>
      <name>Goyal, Manu</name>
    </author>
    <author>
      <name>Vlassenko, Andrei</name>
    </author>
    <author>
      <name>Flores, Shaney</name>
    </author>
    <author>
      <name>Handen, Benjamin L.</name>
    </author>
    <author>
      <name>Head, Elizabeth</name>
    </author>
    <author>
      <name>Keator, David</name>
    </author>
    <author>
      <name>Rafii, Michael S.</name>
    </author>
    <author>
      <name>Lao, Patrick</name>
    </author>
    <author>
      <name>Lai, Florence</name>
    </author>
    <author>
      <name>Rosas, H. Diana</name>
    </author>
    <author>
      <name>Hartley, Sigan L.</name>
    </author>
    <author>
      <name>Zaman, Shahid</name>
    </author>
    <author>
      <name>Brickman, Adam M.</name>
    </author>
    <author>
      <name>Tudorascu, Dana</name>
    </author>
    <author>
      <name>Lee, Joseph H.</name>
    </author>
    <author>
      <name>Allegri, Ricardo Francisco</name>
    </author>
    <author>
      <name>Keefe, Sarah</name>
    </author>
    <author>
      <name>la Fougere, Christian</name>
    </author>
    <author>
      <name>Llibre-Guerra, Jorge</name>
    </author>
    <author>
      <name>Ikeuchi, Takeshi</name>
    </author>
    <author>
      <name>Morris, John C.</name>
    </author>
    <author>
      <name>Roh, Jee Hoon</name>
    </author>
    <author>
      <name>Day, Gregory S.</name>
    </author>
    <author>
      <name>Levin, Johannes</name>
    </author>
    <author>
      <name>Schofield, Peter R.</name>
    </author>
    <author>
      <name>Gordon, Brian A.</name>
    </author>
    <author>
      <name>Benzinger, Tammie L. S.</name>
    </author>
    <author>
      <name>Ances, Beau M.</name>
    </author>
    <id>https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78425</id>
    <updated>2025-12-12T16:04:11Z</updated>
    <published>2025-12-01T00:00:00Z</published>
    <summary type="text">Title: Cross-Sectional FDG in Down Syndrome and Autosomal Dominant Alzheimer&amp;apos;s Disease
Authors: Abdelmoity, Omar; Wisch, Julie K.; Kennedy, James T.; Goyal, Manu; Vlassenko, Andrei; Flores, Shaney; Handen, Benjamin L.; Head, Elizabeth; Keator, David; Rafii, Michael S.; Lao, Patrick; Lai, Florence; Rosas, H. Diana; Hartley, Sigan L.; Zaman, Shahid; Brickman, Adam M.; Tudorascu, Dana; Lee, Joseph H.; Allegri, Ricardo Francisco; Keefe, Sarah; la Fougere, Christian; Llibre-Guerra, Jorge; Ikeuchi, Takeshi; Morris, John C.; Roh, Jee Hoon; Day, Gregory S.; Levin, Johannes; Schofield, Peter R.; Gordon, Brian A.; Benzinger, Tammie L. S.; Ances, Beau M.
Abstract: Objectives: Directly compare the brain glucose patterns seen with [F-18] fluorodeoxyglucose (FDG) positron emission tomography (PET) between 2 genetically determined forms of Alzheimer&amp;apos;s disease: Down syndrome (DS) and autosomal dominant Alzheimer&amp;apos;s disease (ADAD). Methods: Cross-sectional analyses of FDG were performed in individuals with DS (n = 76) from the Alzheimer Biomarker Consortium-Down Syndrome (ABC-DS), ADAD (n = 297), and neurotypical familial controls (n = 188) from the Dominantly Inherited Alzheimer Network (DIAN). Within-group linear regression models and generalized additive models were performed for select regional FDG uptake measures (isthmus cingulate and inferior parietal, precuneus, middle temporal gyrus, and precentral gyrus). Age, sex, apolipoprotein (APOE) epsilon 4 carrier status, and cortical amyloid burden were included within these analyses. Results: Even 20 years before expected onset of clinical symptoms, FDG uptake was lower for DS compared to neurotypical familial controls (p &amp;lt; 0.01). ADAD baseline FDG was similar to neurotypical familial controls until 7 years before expected symptom onset. Both symptomatic individuals with DS and ADAD had lower FDG compared to neurotypical familial controls (p &amp;lt; 0.01). A higher amyloid burden was associated with lower FDG for both genetic forms, with similar rates of decline in FDG uptake for DS and ADAD who were amyloid positive. Interpretation: Brain glucose metabolism is substantially lower for people with DS, even in individuals who are cognitively stable. The patterns of FDG decline are distinct in these 2 genetically determined forms of AD. The diagnostic utility of FDG-PET is specific to the genetic form of AD.</summary>
    <dc:date>2025-12-01T00:00:00Z</dc:date>
  </entry>
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