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Kang, Ju‐Hee

https://orcid.org/0000-0001-5235-8993

Mayo Clinic

Inha University

Citations 2

Exercise as a Therapeutic Strategy for Sarcopenia in Heart Failure: Insights into Underlying Mechanisms
Cho, Jinkyung , Choi, Youngju , Sajgalik, Pavol , No, Mi‐Hyun , Lee, Sang-Hyun , Kim, Sujin , Heo, Jun‐Won , Cho, Eun‐Jeong , Chang, Eunwook , Kang, Ju‐Hee , Kwak, Hyo‐Bum , Park, Dong‐Ho , Schaefer, Jacob J

Cells | October 15, 2020 | Volume: 9 | Issue: 10 | Pages: 2284

10.3390/cells9102284 Get It

Sarcopenia, a syndrome commonly seen in elderly populations, is often characterized by a gradual loss of skeletal muscle, leading to the decline of muscle strength and physical performance. Growing evidence suggests that the prevalence of sarcopenia increases in patients with heart failure (HF), which is a dominant pathogenesis in the aging heart. HF causes diverse metabolic complications that may result in sarcopenia. Therefore, sarcopenia may act as a strong predictor of frailty, disability, and mortality associated with HF. Currently, standard treatments for slowing muscle loss in patients with HF are not available. Therefore, here, we review the pathophysiological mechanisms underlying sarcopenia in HF as well as current knowledge regarding the beneficial effects of exercise on sarcopenia in HF and related mechanisms, including hormonal changes, myostatin, oxidative stress, inflammation, apoptosis, autophagy, the ubiquitin-proteasome system, and insulin resistance.
The Alzheimer's Disease Neuroimaging Initiative 2 Biomarker Core: A review of progress and plans
Korecka, Magdalena , Figurski, Michal, Toledo, Jon B. , Blennow, Kaj , Waligórska, Teresa, Brylska, Magdalena, Fields, Leona, Shah, Nirali, Soares, Holly , Dean, Robert A., Vanderstichele, Hugo, Petersen, Ronald C. , Aisen, Paul , Saykin, Andrew J. , Weiner, Michael W. , Trojanowski, John Q. , Shaw, Leslie M. , Initiative, Alzheimer's Disease Neuroimaging, Kang, Ju‐Hee , Zetterberg, Henrik , Initiative, Alzheimer's Disease Neuroimaging, Saykin, Andrew J

Alzheimer's & Dementia | July 17, 2015 | Volume: 11 | Issue: 7 | Pages: 772-791

10.1016/j.jalz.2015.05.003 Get It

AbstractIntroductionWe describe Alzheimer's Disease Neuroimaging Initiative (ADNI) Biomarker Core progress including: the Biobank; cerebrospinal fluid (CSF) amyloid beta (Aβ1–42), t‐tau, and p‐tau181 analytical performance, definition of Alzheimer's disease (AD) profile for plaque, and tangle burden detection and increased risk for progression to AD; AD disease heterogeneity; progress in standardization; and new studies using ADNI biofluids.MethodsReview publications authored or coauthored by ADNI Biomarker core faculty and selected non‐ADNI studies to deepen the understanding and interpretation of CSF Aβ1–42, t‐tau, and p‐tau181 data.ResultsCSF AD biomarker measurements with the qualified AlzBio3 immunoassay detects neuropathologic AD hallmarks in preclinical and prodromal disease stages, based on CSF studies in non‐ADNI living subjects followed by the autopsy confirmation of AD. Collaboration across ADNI cores generated the temporal ordering model of AD biomarkers varying across individuals because of genetic/environmental factors that increase/decrease resilience to AD pathologies.DiscussionFurther studies will refine this model and enable the use of biomarkers studied in ADNI clinically and in disease‐modifying therapeutic trials.