Piezoelectric properties of aluminum nitride for thin film bulk acoustic wave resonator

Kuangwoo Nam,kuangwoo Nam,Byeongju Ha,심동하,Gwangseo Park,Insang Song,Jaemoon Pak,Yunkwon Park 한국물리학회 2005 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.47 No.2

A film bulk acoustic wave resonator (FBAR) was fabricated by using RF-sputtered aluminum nitride (AlN) between 400 nm-thick molybdenum (Mo) bottom and top electrodes. To reduce the acoustic loss of FBARs, an air gap cavity is fabricated below the membrane by a silicon deep-etch process. The sputtered 950 nm-thick AlN film was oriented in the (002) direction. The FBARs were measured by using a HP 8510C vector network analyzer in a wide frequency range of 0.5 10.5 GHz. A resonance frequency was observed near 2 GHz as well as another, a third mode about 7 GHz. The minimum insertion loss was 0.056 dB at 1858 MHz. An equivalent circuit modeling regarding this FBAR was performed with modified Butterworth Van-Dyke (MBVD) models, wellknown piezoelectric equivalent circuit models. The calculated effective electromechanical coupling coefficient (k2 eff ) was greater than 6.59 %.lf.s

Topographical Visualization of the Reciprocal Projection between the Medial Septum and the Hippocampus in the 5XFAD Mouse Model of Alzheimer’s Disease

Kim, Sujin,Nam, Yunkwon,Jeong, Yu-on,Park, Hyun Ha,Lee, Seong-kyung,Shin, Soo Jung,Jung, Haram,Kim, Byeong-Hyeon,Hong, Sang Bum,Park, Yong Ho,Kim, Jihee,Yu, Jaemin,Yoo, Doo-Han,Park, Sun-Hyun,Jeon, Se MDPI AG 2019 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.20 No.16

<P>It is widely known that the degeneration of neural circuits is prominent in the brains of Alzheimer’s disease (AD) patients. The reciprocal connectivity of the medial septum (MS) and hippocampus, which constitutes the septo-hippocampo-septal (SHS) loop, is known to be associated with learning and memory. Despite the importance of the reciprocal projections between the MS and hippocampus in AD, the alteration of bidirectional connectivity between two structures has not yet been investigated at the mesoscale level. In this study, we adopted AD animal model, five familial AD mutations (5XFAD) mice, and anterograde and retrograde tracers, BDA and DiI, respectively, to visualize the pathology-related changes in topographical connectivity of the SHS loop in the 5XFAD brain. By comparing 4.5-month-old and 14-month-old 5XFAD mice, we successfully identified key circuit components of the SHS loop altered in 5XFAD brains. Remarkably, the SHS loop began to degenerate in 4.5-month-old 5XFAD mice before the onset of neuronal loss. The impairment of connectivity between the MS and hippocampus was accelerated in 14-month-old 5XFAD mice. These results demonstrate, for the first time, topographical evidence for the degradation of the interconnection between the MS and hippocampus at the mesoscale level in a mouse model of AD. Our results provide structural and functional insights into the interconnectivity of the MS and hippocampus, which will inform the use and development of various therapeutic approaches that target neural circuits for the treatment of AD.</P>

Proteomic analysis for the effects of non-saponin fraction with rich polysaccharide from Korean Red Ginseng on Alzheimer's disease in a mouse model

Sujin Kim,Yunkwon Nam,Min-jeong Kim,Seung-hyun Kwon,Junhyeok Jeon,Soo Jung Shin,Soyoon Park,Sungjae Chang,Hyun Uk Kim,Yong Yook Lee,Hak Su Kim,Minho Moon The Korean Society of Ginseng 2023 Journal of Ginseng Research Vol.47 No.2

Background: The most common type of dementia, Alzheimer's disease (AD), is marked by the formation of extracellular amyloid beta (Aβ) plaques. The impairments of axons and synapses appear in the process of Aβ plaques formation, and this damage could cause neurodegeneration. We previously reported that non-saponin fraction with rich polysaccharide (NFP) from Korean Red Ginseng (KRG) showed neuroprotective effects in AD. However, precise molecular mechanism of the therapeutic effects of NFP from KRG in AD still remains elusive. Methods: To investigate the therapeutic mechanisms of NFP from KRG on AD, we conducted proteomic analysis for frontal cortex from vehicle-treated wild-type, vehicle-treated 5XFAD mice, and NFP-treated 5XFAD mice by using nano-LC-ESI-MS/MS. Metabolic network analysis was additionally performed as the effects of NFP appeared to be associated with metabolism according to the proteome analysis. Results: Starting from 5,470 proteins, 2,636 proteins were selected for hierarchical clustering analysis, and finally 111 proteins were further selected for protein-protein interaction network analysis. A series of these analyses revealed that proteins associated with synapse and mitochondria might be linked to the therapeutic mechanism of NFP. Subsequent metabolic network analysis via genome-scale metabolic models that represent the three mouse groups showed that there were significant changes in metabolic fluxes of mitochondrial carnitine shuttle pathway and mitochondrial beta-oxidation of polyunsaturated fatty acids. Conclusion: Our results suggested that the therapeutic effects of NFP on AD were associated with synaptic- and mitochondrial-related pathways, and they provided targets for further rigorous studies on precise understanding of the molecular mechanism of NFP.

Characterization of age- and stage-dependent impaired adult subventricular neurogenesis in 5XFAD mouse model of Alzheimer’s disease

Hyun Ha Park,Byeong-Hyeon Kim,Seol Hwa Leem,Yong Ho Park,Hyang-Sook Hoe,Yunkwon Nam,Sujin Kim,Soo Jung Shin,Minho Moon 생화학분자생물학회 2023 BMB Reports Vol.56 No.9

Alzheimer’s disease (AD) is a progressive neurodegenerative diseasecharacterized by cognitive decline. Several recent studiesdemonstrated that impaired adult neurogenesis could contributeto AD-related cognitive impairment. Adult subventricularzone (SVZ) neurogenesis, which occurs in the lateral ventricles,plays a crucial role in structural plasticity and neural circuitmaintenance. Alterations in adult SVZ neurogenesis are earlyevents in AD, and impaired adult neurogenesis is influencedby the accumulation of intracellular Aβ. Although Aβ-overexpressingtransgenic 5XFAD mice are an AD animal model wellrepresentative of Aβ-related pathologies in the brain, the characterizationof altered adult SVZ neurogenesis following ADprogression in 5XFAD mice has not been thoroughly examined. Therefore, we validated the characterization of adult SVZ neurogenesischanges with AD progression in 2-, 4-, 8-, and 11-montholdmale 5XFAD mice. We first investigated the Aβ accumulationin the SVZ using the 4G8 antibody. We observed intracellularAβ accumulation in the SVZ of 2-month-old 5XFADmice. In addition, 5XFAD mice exhibited significantly increasedAβ deposition in the SVZ with age. Next, we performed a histologicalanalysis to investigate changes in various phases of adultneurogenesis, such as quiescence, proliferation, and differentiation,in SVZ. Compared to age-matched wild-type (WT) mice,quiescent neural stem cells were reduced in 5XFAD mice from2-11 months of age. Moreover, proliferative neural stem cellswere decreased in 5XFAD mice from 2 to 8 months of age. Furthermore, differentiations of neuroblasts were diminished in5XFAD mice from 2-11 months of age. Intriguingly, we foundthat adult SVZ neurogenesis was reduced with aging in healthymice. Taken together, our results revealed that impairment ofadult SVZ neurogenesis appears with aging or AD progression.

Jowiseungchungtang Inhibits Amyloid-β Aggregation and Amyloid-β-Mediated Pathology in 5XFAD Mice

Shin, Soo Jung,Jeong, Yu-on,Jeon, Seong Gak,Kim, Sujin,Lee, Seong-kyung,Nam, Yunkwon,Park, Yong Ho,Kim, Dabi,Lee, Youn Seok,Choi, Hong Seok,Kim, Jin-il,Kim, Jwa-Jin,Moon, Minho MDPI AG 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.12

<P>Alzheimer’s disease (AD) is a neurodegenerative disease, which is accompanied by memory loss and cognitive dysfunction. Although a number of trials to treat AD are in progress, there are no drugs available that inhibit the progression of AD. As the aggregation of amyloid-β (Aβ) peptides in the brain is considered to be the major pathology of AD, inhibition of Aβ aggregation could be an effective strategy for AD treatment. Jowiseungchungtang (JWS) is a traditional oriental herbal formulation that has been shown to improve cognitive function in patients or animal models with dementia. However, there are no reports examining the effects of JWS on Aβ aggregation. Thus, we investigated whether JWS could protect against both Aβ aggregates and Aβ-mediated pathology such as neuroinflammation, neurodegeneration, and impaired adult neurogenesis in 5 five familial Alzheimer’s disease mutations (5XFAD) mice, an animal model for AD. In an in vitro thioflavin T assay, JWS showed a remarkable anti-Aβ aggregation effect. Histochemical analysis indicated that JWS had inhibitory effects on Aβ aggregation, Aβ-induced pathologies, and improved adult hippocampal neurogenesis in vivo. Taken together, these results suggest the therapeutic possibility of JWS for AD targeting Aβ aggregation, Aβ-mediated neurodegeneration, and impaired adult hippocampal neurogenesis.</P>