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Shin, Jin A.,Jeong, Sae Im,Kim, Hye Won,Jang, Gyeonghui,Ryu, Dong-Ryeol,Ahn, Young-Ho,Choi, Ji Ha,Choi, Youn-Hee,Park, Eun-Mi PERGAMON PRESS LTD 2018 NEUROBIOLOGY OF AGING Vol. No.
<P><B>Abstract</B></P> <P>The adenosine triphosphate–binding cassette efflux transporter ABCG2, which is located in the blood-brain barrier limits the entry of endogenous compounds and xenobiotics into the brain, and its expression and activity are regulated by estrogen. This study was aimed to define the role of ABCG2 in estrogen-mediated neuroprotection against ischemic injury. ABCG2 protein levels before and after ischemic stroke were increased in the brain of female mice by ovariectomy, which were reversed by estrogen replacement. In brain endothelial cell line bEnd.3, estrogen reduced the basal ABCG2 protein level and efflux activity and protected cells from ischemic injury without inducing ABCG2 expression. When bEnd.3 cells were transfected with ABCG2 small interfering RNA, ischemia-induced cell death was reduced, and the intracellular concentration of glutathione, an antioxidant that is transported by ABCG2, was increased. In addition, after ischemic stroke in ovariectomized mice, estrogen prevented the reduction of intracellular glutathione level in brain microvessels. These data suggested that the suppression of ABCG2 by estrogen is involved in neuroprotection against ischemic injury by increasing intracellular glutathione, and that the modulation of ABCG2 activity offers a therapeutic target for brain diseases in estrogen-deficient aged women.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Diaminodiphenyl sulfone-induced parkin ameliorates age-dependent dopaminergic neuronal loss
Lee, Y.I.,Kang, H.,Ha, Y.W.,Chang, K.Y.,Cho, S.C.,Song, S.O.,Kim, H.,Jo, A.,Khang, R.,Choi, J.Y.,Lee, Y.,Park, S.C.,Shin, J.H. PERGAMON PRESS LTD 2016 NEUROBIOLOGY OF AGING Vol.41 No.-
During normal aging, the number of dopaminergic (DA) neurons in the substantia nigra progressively diminishes, although massive DA neuronal loss is a hallmark sign of Parkinson's disease. Unfortunately, there is little known about the molecular events involved in age-related DA neuronal loss. In this study, we found that (1) the level of parkin was decreased in the cerebellum, brain stem, substantia nigra, and striatum of aged mice, (2) diaminodiphenyl sulfone (DDS) restored the level of parkin, (3) DDS prevented age-dependent DA neuronal loss, and (4) DDS protected SH-SY5Y cells from 1-methyl-4-phenylpyridinium and hydrogen peroxide. Furthermore, pretreatment and/or post-treatment of DDS in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease model attenuated DA neuronal loss and restored motor behavior. DDS transcriptionally activated parkin via protein kinase RNA-like endoplasmic reticulum kinase-activating transcription factor 4 signaling and DDS not only failed to induce parkin expression but also failed to rescue SH-SY5Y cells from 1-methyl-4-phenylpyridinium in the absence of ATF4. Herein, we demonstrated for the first time that DDS increased parkin level and served as a neuroprotective agent for age-dependent DA neuronal loss. Thus, DDS may be a potential therapeutic agent for age-related neurodegeneration.
Baek, Young Sook,Lee, Sang Hoon,Chang, Tae Soo PERGAMON PRESS LTD 2017 QUATERNARY INTERNATIONAL Vol.459 No.-
<P><B>Abstract</B></P> <P>Over the past two decades, tidal flats in the west coast of Korea (eastern Yellow Sea) have been extensively investigated to reveal sedimentation and stratigraphic evolution coupled with sea level changes. In spite of such efforts, their sedimentary record and evolution pattern particularly in the deeper subtidal area are relatively little documented. To expand and fulfill our knowledge on sedimentation history from last interglacial to the Holocene, three drilled cores (up to ca. 28 m in length) and Chirp seismic profiles obtained from the subtidal zones along the southwestern coast of Korea were examined, with supplementary OSL and <SUP>14</SUP>C-AMS age dates. Based on the sedimentary facies analysis correlated with seismic units, the subtidal deposits can be divided into four units: Unit I) basal fluvial deposit (MIS 6?), Unit II) tidal deposits (MIS 5e), Unit III) transition deposits between salt marsh and oxidized inland coastal dune (early Holocene), and Unit IV) Holocene tidal deposits, in ascending order. These units can be then grouped into two sedimentary sequences, a lower sequence S1 (Unit I and II) and an upper S2 (Unit III and IV) separated by an unconformable surface, being responded to two cycles in sea-level fluctuations. Each sequence started with non-marine deposits formed during lowstand in sea-level, and then overlain by tidal successions deposited during transgression. The feature thus indicates two tidal deposits, i.e., last interglacial and the Holocene in ages, preserved in the macrotidal west coast of Korea, possibly being major constituents of coastal successions to be survived in the records. This can be used to correlate with other marine strata in the western (Chinese) Yellow Sea since the last interglacial.</P>
Cho, Hanna,Seo, Sang Won,Choi, Jae Yong,Lee, Hye Sun,Ryu, Young Hoon,Lee, Myung Sik,Na, Duk L.,Kim, Hee Jin,Lyoo, Chul Hyoung PERGAMON PRESS LTD 2018 NEUROBIOLOGY OF AGING Vol. No.
<P><B>Abstract</B></P> <P>Behavioral variant frontotemporal dementia (bvFTD) is the most common form of frontotemporal dementia, and tau pathology can be found in 40%–50% of bvFTD patients. In this study, we sought to investigate <SUP>18</SUP>F-flortaucipir-binding patterns and their correlates in clinically diagnosed bvFTD patients by comparing with results for Alzheimer's disease (AD) patients. We enrolled 20 bvFTD, 20 AD, and 20 age-matched healthy subjects who underwent neuropsychological tests, magnetic resonance imaging, and tau positron emission tomography scans with <SUP>18</SUP>F-flortaucipir. Regional standardized uptake value ratios for the cerebral cortex and underlying white matter were compared between the 2 groups. The bvFTD patients showed increased <SUP>18</SUP>F-flortaucipir binding in the putamen and globus pallidus when compared to the healthy controls. In addition, bvFTD was associated with increased binding in the white matter regions underlying the frontal, anterior cingulate, and insula cortices. The bvFTD patients may exhibit predominantly subcortical <SUP>18</SUP>F-flortaucipir-binding pattern that is distinct from the patterns seen in AD patients. We hypothesize that the clinical characteristics of bvFTD patients may be attributable to the dysfunctional frontal-subcortical networks. However, concerns remain regarding unknown “off-target” binding in the white matter and the basal ganglia.</P>
Kim, M.J.,Seo, M.,Oh, C.S.,Chai, J.Y.,Lee, J.,Kim, G.j.,Ma, W.Y.,Choi, S.J.,Reinhard, K.,Araujo, A.,Shin, D.H. PERGAMON PRESS LTD 2016 QUATERNARY INTERNATIONAL Vol.405 No.2
<P>Due to paleoparasitology's relatively late beginnings, the fundamental data necessary for any reasonably complete understanding of parasitic infection patterns in Korean history remains insufficient. Especially with respect to ancient samples dating to before the Joseon Dynasty (1392-1910 CE), few cases have been analyzed by parasitological techniques. In the present study, we therefore undertook a series of paleoparasitological examinations of archaeological samples from the ancient Silla Kingdom (57 BCE-935 CE). Specifically, in soil samples obtained from shell midden and mountain top fortress sites, we observed Ascaris lumbricoides, Trichuris trichiura, Dicrocoelid and Taenia sp. eggs. The results of our current investigation of strata and samples from the prosperous first-millennium era of the Silla Kingdom are encouraging for a comprehensive understanding of the parasitic infection patterns in the earlier days of Korean history that could not be obtained by any previous studies. (C) 2015 Elsevier Ltd and INQUA. All rights reserved.</P>
Age-related changes in pial arterial structure and blood flow in mice
Kang, H.M.,Sohn, I.,Jung, J.,Jeong, J.W.,Park, C. PERGAMON PRESS LTD 2016 NEUROBIOLOGY OF AGING Vol. No.
Age-related cerebral blood flow decreases are thought to deteriorate cognition and cause senescence, although the related mechanism is unclear. To investigate the relationships between aging and changes in cerebral blood flow and vasculature, we obtained fluorescence images of young (2-month-old) and old (12-month-old) mice using indocyanine green (ICG). First, we found that the blood flow in old mice's brains is lower than that in young mice and that old mice had more curved pial arteries and fewer pial artery junctions than young mice. Second, using Western blotting, we determined that the ratio of collagen to elastin (related to cerebral vascular wall distensibility) increased with age. Finally, we found that the peak ICG intensity and blood flow index decreased, whereas the mean transit time increased, with age in the middle cerebral artery and superior sagittal sinus. Age-related changes in pial arterial structure and composition, concurrent with the observed changes in the blood flow parameters, suggest that age-related changes in the cerebral vasculature structure and distensibility may induce altered brain blood flow.
Byun, Min Soo,Kim, Hyun Jung,Yi, Dahyun,Choi, Hyo Jung,Baek, Hyewon,Lee, Jun Ho,Choe, Young Min,Sohn, Bo Kyung,Lee, Jun-Young,Lee, Younghwa,Ko, Hyunwoong,Kim, Yu Kyeong,Lee, Yun-Sang,Sohn, Chul-Ho,Woo PERGAMON PRESS LTD 2017 NEUROBIOLOGY OF AGING Vol. No.
<P><B>Abstract</B></P> <P>We tested the hypothesis that lower insulin or higher glycated hemoglobin (HbA1c) levels in blood are associated with increased cerebral beta amyloid (Aβ) deposition and neurodegeneration in nondiabetic cognitively normal (CN) older adults. A total of 205 nondiabetic CN older adults underwent comprehensive clinical assessment, [<SUP>11</SUP>C]Pittsburgh compound B (PiB)-positron emission tomography (PET), [<SUP>18</SUP>F]fluorodeoxyglucose-PET, magnetic resonance imaging, and blood sampling for fasting insulin and HbA1c measurement. Lower blood insulin was significantly associated with increased Aβ positivity rates and decreased cerebral glucose metabolism in the AD-signature region. In contrast, higher HbA1c levels were not associated with Aβ positivity rates but were significantly associated with higher rates of having neurodegeneration in the AD-signature regions. Our results suggest different roles of insulin and HbA1c in AD pathogenesis, in that decreased blood insulin below optimal levels may contribute to increasing cerebral Aβ deposition and neurodegeneration whereas impaired glycemic control may aggravate neurodegeneration through a nonamyloid mechanism in nondiabetic CN older adults.</P>