17 results on '"Choi, In-Gyu"'
Search Results
2. Rejuvenating aged microglia by p16ink4a-siRNA-loaded nanoparticles increases amyloid-β clearance in animal models of Alzheimer's disease.
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Shin, Hyo Jung, Kim, In Soo, Choi, Seung Gyu, Lee, Kayoung, Park, Hyewon, Shin, Juhee, Kim, Dayoung, Beom, Jaewon, Yi, Yoon Young, Gupta, Deepak Prasad, Song, Gyun Jee, Chung, Won-Suk, Lee, C. Justin, and Kim, Dong Woon
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ALZHEIMER'S disease ,CYCLIN-dependent kinases ,MICROGLIA ,CYCLIN-dependent kinase inhibitors ,AMYLOID beta-protein precursor ,P16 gene ,SMALL interfering RNA ,CELL cycle ,NANOMEDICINE - Abstract
Age-dependent accumulation of amyloid plaques in patients with sporadic Alzheimer's disease (AD) is associated with reduced amyloid clearance. Older microglia have a reduced ability to phagocytose amyloid, so phagocytosis of amyloid plaques by microglia could be regulated to prevent amyloid accumulation. Furthermore, considering the aging-related disruption of cell cycle machinery in old microglia, we hypothesize that regulating their cell cycle could rejuvenate them and enhance their ability to promote more efficient amyloid clearance. First, we used gene ontology analysis of microglia from young and old mice to identify differential expression of cyclin-dependent kinase inhibitor 2A (p16
ink4a ), a cell cycle factor related to aging. We found that p16ink4a expression was increased in microglia near amyloid plaques in brain tissue from patients with AD and 5XFAD mice, a model of AD. In BV2 microglia, small interfering RNA (siRNA)-mediated p16ink4a downregulation transformed microglia with enhanced amyloid phagocytic capacity through regulated the cell cycle and increased cell proliferation. To regulate microglial phagocytosis by gene transduction, we used poly (D,L-lactic-co-glycolic acid) (PLGA) nanoparticles, which predominantly target microglia, to deliver the siRNA and to control microglial reactivity. Nanoparticle-based delivery of p16ink4a siRNA reduced amyloid plaque formation and the number of aged microglia surrounding the plaque and reversed learning deterioration and spatial memory deficits. We propose that downregulation of p16ink4a in microglia is a promising strategy for the treatment of Alzheimer's disease. [ABSTRACT FROM AUTHOR]- Published
- 2024
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3. Interaction Between a High-Fat Diet and Tau Pathology in Mice: Implications for Alzheimer's Disease.
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Jang, Yu Jung, Choi, Min Gyu, Yoo, Byung Jae, Lee, Kyeong Jae, Jung, Won Beom, Kim, Seong-Gi, and Park, Sun Ah
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ALZHEIMER'S disease , *HIGH-fat diet , *DISEASE risk factors , *FUNCTIONAL magnetic resonance imaging , *TAU proteins - Abstract
Background: Obesity is a modifiable risk factor for Alzheimer's disease (AD). However, its relation with tau pathology (i.e., aberrant tau protein behavior in tauopathies such as AD) has been inconclusive. Objective: This study investigated the interaction between a high-fat diet (HFD) and tau pathology in adult male mice. Methods: Transgenic mice overexpressing human P301S Tau (those with the pathology) and wild-type (WT) littermates were subjected to behavioral tests, functional magnetic resonance imaging (fMRI), diffusion tensor imaging (DTI), and western blotting analysis to investigate the effects of prolonged HFD versus regular diet during adulthood. Results: HFD increased body weight in both WT and P301S mice but had minimal effect on blood glucose levels. The brain response to HFD was tau genotype-specific. WT mice exhibited decreased recognition memory and enhanced network connectivity in fMRI, while P301S mice exhibited white matter tract disorganization in DTI as the sole significant finding. The reduction of insulin receptor β, insulin downstream signaling, neuronal nuclear protein, CD68-positive phagocytic activity, and myelin basic protein level were confined to the cortex of WT mice. In contrast to P301S mice, WT mice showed significant changes in the tau protein and its phosphorylation levels along with increased soluble neurofilament light levels in the hippocampus. Conclusions: HFD-induced brain dysfunction and pathological changes were blunted in mice with the pathology and more profound in healthy mice. Our findings highlight the need to consider this interaction between obesity and tau pathology when tailoring treatment strategies for AD and other tauopathies. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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4. Aerial part of Houttuynia cordata reverses memory impairment by regulating amyloid beta accumulation and neuroinflammation in Alzheimer's disease model.
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Ju, In Gyoung, Lee, Seungmin, Choi, Jin Gyu, Kim, Namkwon, Huh, Eugene, Lee, Jong Kil, and Oh, Myung Sook
- Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disease characterized by amyloid‐β (Aβ) deposition, accompanied by neuroinflammation and memory dysfunction. Houttuyniae Herba (aerial parts of Houttuynia cordata, also known as fish mint; HH), an herbal medicine traditionally used to treat fever, urinary disorders, and pus, is revealed to protect neurons from Aβ toxicity and regulate cholinergic dysfunction in AD models. In this study, we aimed to investigate the effects of HH on excessive accumulation of Aβ followed by neuroinflammation, synaptic degeneration, and memory impairment. Two‐month‐old 5xFAD transgenic mice were administered HH at 100 mg/kg for 4 months. We observed that HH treatment ameliorated memory impairment and reduced Aβ deposits in the brains of the mice. HH directly inhibited Aβ aggregation in vitro using the Thioflavin T assay and indirectly suppressed the amyloidogenic pathway by increasing alpha‐secretase expression in the mice brain. In addition, HH exerted antineuroinflammatory effects by reducing of glial activation and p38 phosphorylation. Moreover, HH treatment increased the expression of synaptophysin, a presynaptic marker protein. Overall, HH alleviates memory impairment in AD by facilitating nonamyloidogenic pathway and inhibiting neuroinflammation. Therefore, we suggest that HH can be a promising herbal drug for patients with AD requiring multifaceted improvement. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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5. A novel nutritional mixture, MBN, prevents memory impairment via inhibiting NLRP3 inflammasome formation in 5xFAD transgenic mice.
- Author
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Kim, Namkwon, Choi, Jin Gyu, Ju, In Gyoung, Ju, Yeon-Joo, Yim, Sung-Vin, Lee, Jong Kil, and Oh, Myung Sook
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GINKGO , *MEMORY disorders , *MICE , *TRANSGENIC mice , *NLRP3 protein , *INFLAMMASOMES , *ORAL drug administration , *ALZHEIMER'S disease - Abstract
Amyloid beta (Aβ)-induced abnormal neuroinflammation is recognized as a major pathological factor of Alzheimer's disease (AD), which results in memory impairment. Inhibition of excessive neuroinflammation mediated by Aβ is considered a promising strategy to ameliorate AD symptoms. To regulate the inflammatory response, nutritional and dietary supplements have been used for centuries. Based on this idea, we investigated whether MBN, a novel nutritional mixture including cassia bark, turmeric root, and ginkgo leaf, can prevent AD progression through neuroinflammatory regulation. MBN (10, 30, or 100 μg/ml) and Aβ1-42 monomer were incubated together, and the degree of Aβ aggregation was measured using Thioflavin T assay. The effects of MBN on Aβ pathology in vivo were evaluated by orally administering MBN (40 mg/kg/day for 16 weeks) to five familial AD (5xFAD) mice. We found that treatment with MBN inhibited Aβ aggregation in vitro. Next, MBN treatment significantly inhibited the activation of microglia induced by aggregated Aβ in 5xFAD mice. Caspase-1 activation, which plays an important role in the maturation of interleukin-1β, was markedly reduced by MBN. We also found that oral administration of MBN in 5xFAD mice alleviated memory decline. Taken together, our findings demonstrate that MBN suppresses neuroinflammation by downregulating the caspase-1 expression, thereby ameliorating memory impairment in 5xFAD mice. Based on these results, we suggest that MBN may be a preventive and therapeutic supplement for AD through the regulation of neuroinflammation. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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6. Harnessing Intramolecular Rotation To Enhance Two‐photon Imaging of Aβ Plaques through Minimizing Background Fluorescence.
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Shin, Jinwoo, Verwilst, Peter, Choi, Hayoung, Kang, Sangrim, Han, Jiyou, Kim, Na Hee, Choi, Jin Gyu, Oh, Myung Sook, Hwang, Ji Sun, Kim, Dokyoung, Mook‐Jung, Inhee, and Kim, Jong Seung
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FLUORESCENCE ,BIOFLUORESCENCE ,INTRAMOLECULAR proton transfer reactions ,AMYLOID plaque ,ALZHEIMER'S disease ,ROTATIONAL motion - Abstract
The aggregation of amyloid beta (Aβ) proteins in senile plaques is a critical event during the development of Alzheimer's disease, and the postmortem detection of Aβ‐rich proteinaceous deposits through fluorescent staining remains one of the most robust diagnostic tools. In animal models, fluorescence imaging can be employed to follow the progression of the disease, and among the different imaging methods, two‐photon microscopy (TPM) has emerged as one of the most powerful. To date, several near‐infrared‐emissive two‐photon dyes with a high affinity for Aβ fibrils have been developed, but there has often been a tradeoff between excellent two‐photon cross‐sections and large fluorescence signal‐to‐background ratios. In the current work, we introduced a twisted intramolecular charge state (TICT)‐based de‐excitation pathway, which results in a remarkable fluorescence increase of around 167‐fold in the presence of Aβ fibrils, while maintaining an excellent two‐photon cross section, thereby enabling high‐contrast ex vivo and in vivo TPM imaging. Overall, the results suggest that adopting TICT de‐excitation in two‐photon fluorophores may represent a general method to overcome the tradeoff between probe brightness and signal‐to‐background ratio. Do the twist: A twisted intramolecular charge state (TICT)‐based de‐excitation pathway was introduced in an Aβ dye. This gave a 167‐fold fluorescence increase in the presence of Aβ fibrils, while maintaining an excellent two‐photon cross‐section, thereby enabling high‐contrast two‐photon microscopy (TPM) imaging. TICT de‐excitation in two‐photon fluorophores may represent a general method to overcome the tradeoff between brightness and signal‐to‐background ratio. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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7. Optimized-SopungSunkiwon, a Herbal Formula, Attenuates Aβ Oligomer-Induced Neurotoxicity in Alzheimer’s Disease Models.
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Choi, Jin Gyu, Kim, Sun Yeou, Kim, Jong Woo, and Oh, Myung Sook
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PHYTOTHERAPY , *REACTIVE oxygen species , *ALZHEIMER'S disease , *ANIMAL experimentation , *APOPTOSIS , *BIOLOGICAL models , *ASIAN medicine , *MICE , *NEURONS , *NEUROTOXICOLOGY , *NITRIC oxide , *POLYMERS , *SYNDROMES , *TREATMENT effectiveness , *NEUROPROTECTIVE agents , *IN vitro studies , *IN vivo studies - Abstract
Alzheimer’s disease (AD), the most common form of dementia, is an age-related neurodegenerative disease that is characterized by memory dysfunction, neuronal cell damage, and neuroinflammation. It is believed that AD-related pathology is mostly due to the overproduction of Aβ, especially the oligomeric form (AβO), in the brain. Evidence of the effects of multifunctional medicinal herbs in the treatment of AD has been steadily increasing. Optimized-SopungSunkiwon (OSS), a multiherbal formulation that is composed of six medicinal herbs derived from SopungSunkiwon, is a traditional medicine that is prescribed for neurodegenerative disorders in elderly patients. We previously reported that OSS showed an antiamnesic and memory enhancing effect in mice, but it is unknown whether OSS has a protective effect against AβO neurotoxicity. In this study, we investigated the effects of OSS in AD models induced by AβO in vitro and in vivo. We found that OSS protected neuronal cells and inhibited the generation of nitric oxide and reactive oxygen species against AβO toxicity in vitro. These results were confirmed by in vivo data that oral administration of OSS for 14 days attenuated memory impairments and neuronal cell death by modulating gliosis, glutathione depletion, and synaptic damage in the mouse hippocampus induced by AβO. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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8. White Ginseng Protects Mouse Hippocampal Cells Against Amyloid-Beta Oligomer Toxicity.
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Choi, Jin Gyu, Kim, Namkwon, Huh, Eugene, Lee, Hwan, Oh, Myeong Hwan, Park, Jong Dae, Pyo, Mi Kyung, and Oh, Myung Sook
- Abstract
Amyloid-beta oligomer (AβO) is a soluble oligomer form of the Aβ peptide and the most potent amyloid-beta form that induces neuronal damage in Alzheimer's disease. We investigated the effect of dried white ginseng extract (WGE) on neuronal cell damage and memory impairment in intrahippocampal AβO (10 μM)-injected mice. Mice were treated with WGE (100 and 500 mg/kg/day, p.o.) for 12 days after surgery. WGE improved memory impairment by inhibiting hippocampal cell death caused by AβO. In addition, AβO-injected mice treated with WGE showed restoration of reduced synaptophysin and choline acetyltransferase intensity and lower levels of ionized calcium-binding adaptor molecule 1 in the hippocampus compared with those of vehicle-treated controls. These results suggest that WGE reverses memory impairment in Alzheimer's disease by attenuating neuronal damage and neuroinflammation in the AβO-injected mouse hippocampus. Copyright © 2017 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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9. An Optimized Combination of Ginger and Peony Root Effectively Inhibits Amyloid-β Accumulation and Amyloid-β-Mediated Pathology in AβPP/PS1 Double-Transgenic Mice.
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Soonmin Lim, Jin Gyu Choi, Minho Moon, Hyo Geun Kim, Wonil Lee, Hyoung-rok Bak, Hachang Sung, Chi Hye Park, Sun Yeou Kim, Myung Sook Oh, Lim, Soonmin, Choi, Jin Gyu, Moon, Minho, Kim, Hyo Geun, Lee, Wonil, Bak, Hyoung-Rok, Sung, Hachang, Park, Chi Hye, Kim, Sun Yeou, and Oh, Myung Sook
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AMYLOID ,ALZHEIMER'S disease ,HERBAL medicine ,LABORATORY mice ,INFLAMMATION ,DIAGNOSIS ,BIOTHERAPY ,ANALYSIS of variance ,ANIMAL experimentation ,BIOLOGICAL models ,CYTOSKELETAL proteins ,DOSE-effect relationship in pharmacology ,GINGER ,MEMBRANE proteins ,MICE ,GENETIC mutation ,OXIDOREDUCTASES ,PEPTIDES ,PLANTS ,PROTEIN precursors - Abstract
The progressive aggregation of amyloid-β protein (Aβ) into senile plaques is a major pathological factor of Alzheimer's disease (AD) and is believed to result in memory impairment. We aimed to investigate the effect of an optimized combination of ginger and peony root (OCGP), a standardized herbal mixture of ginger and peony root, on Aβ accumulation and memory impairment in amyloid-β protein precursor (AβPP)/presenilin 1 (PS1) double-transgenic mice. In an in vitro thioflavin T fluorescence assay, 100 μg/ml OCGP inhibited Aβ accumulation to the same extent as did 10 μM curcumin. Furthermore, AβPP/PS1 double-transgenic mice treated with OCGP (50 or 100 mg/kg/day given orally for 14 weeks) exhibited reduced Aβ plaque accumulation in the hippocampus and lower levels of glial fibrillary acid protein and cyclooxygease-2 expression compared with vehicle-treated controls. These results suggest that OCGP may prevent memory impairment in AD by inhibiting Aβ accumulation and inflammation in the brain. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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10. Bombycis excrementum Reduces Amyloid-β Oligomer-Induced Memory Impairments, Neurodegeneration, and Neuroinflammation in Mice.
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Moon, Minho, Choi, Jin Gyu, Kim, Sun Yeou, and Oh, Myung Sook
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ALZHEIMER'S disease research , *AMYLOID beta-protein , *OLIGOMERS , *COGNITION disorders , *NEUROPROTECTIVE agents , *ANIMAL droppings , *SILKWORMS ,THERAPEUTIC use of plant extracts - Abstract
Alzheimer's disease (AD) is the most common cause of progressive dementia and is characterized by memory impairments, neuronal death, and neuroinflammation. AD-related pathophysiology is caused primarily by the presence of amyloid-β oligomers (AβO). Recently, an increased focus has been directed toward natural compounds or medicinal extracts for the treatment of AD. Extracts from Bombycis excrementum (BE), which is composed of various bioactive constituents and mulberry leaves (the preferred food of silkworms), have been shown to possess anti-inflammatory, anti-diabetic, and anti-oxidative effects. Additionally, mulberry leaves exert anti-amyloidogenic action and neuroprotective effects against Aβ peptides but it is unknown whether BE has a therapeutic effect on AD-related pathologies. Therefore, the present study examined whether BE inhibits AβO-induced memory loss, neuronal death, and inflammation. Behavioral tests revealed that BE significantly ameliorated AβO-induced memory impairments and inhibited AβO-induced neuronal loss in cultured cells and the brains of mice. BE also significantly inhibited microgliosis and astrogliosis following intra-hippocampal AβO injections in mice. Furthermore, BE significantly attenuated the release of nitric oxide from microglia and reduced AβO-induced S100-β cytokine release from activated astrocytes. These results suggest that BE may be a candidate agent for the treatment of AD. [ABSTRACT FROM AUTHOR]
- Published
- 2014
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11. T1-weighted Axial Visual Rating Scale for an Assessment of Medial Temporal Atrophy in Alzheimer's Disease.
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Kim, Geon Ha, Kim, Jung-Eun, Choi, Kyoung-Gyu, Lim, Soo Mee, Lee, Jong-Min, Na, Duk L., and Jeong, Jee Hyang
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VISION research ,ALZHEIMER'S disease research ,COGNITIVE ability ,HIPPOCAMPUS physiology ,DEMENTIA research - Abstract
Background: The most-widely used visual rating scale (VRS) for medial temporal atrophy is the T1-weighted (T1W) coronal VRS developed by Scheltens et al. However, it is often difficult to use the T1W-coronal VRS in cases with limitations in obtaining T1W-coronal images. To overcome this issue, we modified the T1W-coronal VRS onto the axial plane. Objective: The purposes of this study were to validate our T1W-axial VRS by examining its compatibility with the original T1W-coronal VRS and by investigating the correlation with the cognitive functions and hippocampal volumes. Methods: Participants were 50 patients with Alzheimer's disease dementia and 30 elderly with normal cognition. We transposed each component of the T1W-coronal VRS onto T1W-axial images (i.e., the largest height of the hippocampal formation into the width of the medial temporal lobe). The compatibility of T1W-axial VRS with T1W-coronal one was determined using the kappa value. The correlations of T1W-axial VRS with cognitive performance or the hippocampal volumes were analyzed with age, gender, and education as covariates. Results: The kappa value between the T1W-axial and T1W-coronal VRS was 0.772 (p < 0.045). The T1W-axial VRS showed a significant correlation with the scores of cognitive functions, including verbal memory tests (-0.601, p < 0.001 for the left). Furthermore, the T1W-axial VRS also correlated well with hippocampal volumes (-0.576, p < 0.001). Conclusions: The T1W-axial VRS showed good agreement with T1W-coronal VRS and correlated well with cognitive functions as well as hippocampal volumes, which suggests that the T1-axial VRS may replace the original T1W-coronal one. [ABSTRACT FROM AUTHOR]
- Published
- 2014
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12. Gami-Chunghyuldan ameliorates memory impairment and neurodegeneration induced by intrahippocampal Aβ1–42 oligomer injection
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Choi, Jin Gyu, Moon, Minho, Kim, Hyo Geun, Mook-Jung, Inhee, Chung, Sun Yong, Kang, Tong Ho, Kim, Sun Yeou, Lee, Eunjoo H., and Oh, Myung Sook
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NEURODEGENERATION , *HIPPOCAMPUS (Brain) , *MEMORY , *OLIGOMERS , *AMYLOID beta-protein , *COGNITION disorders , *ALZHEIMER'S disease , *LABORATORY mice - Abstract
Abstract: Soluble oligomeric forms of amyloid beta (AβO) are regarded as a main cause of synaptic and cognitive dysfunction in Alzheimer’s disease (AD) and have been a primary target in the development of drug treatments for AD. The present study utilized a mouse model of AD induced by intrahippocampal injection of AβO (10μM) to investigate the effects of Gami-Chunghyuldan (GCD), a standardized multi-herbal medicinal formula, on the presentation of memory deficits and neurohistological pathogenesis. GCD (10 and 50mg/kg/day, 5days, p.o.) improved AβO-induced memory impairment as well as reduced neuronal cell death, astrogliosis, and microgliosis in the hippocampus. In addition, GCD prevented AβO-triggered synaptic disruption and cholinergic fiber loss. These results suggest that GCD may be useful in the prevention and treatment of AD. [Copyright &y& Elsevier]
- Published
- 2011
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13. Effects of optimized-SopungSunkiwon on memory impairment and enhancement
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Choi, Jin Gyu, Yang, Woong Mo, Kang, Tong Ho, and Oh, Myung Sook
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MEMORY disorders , *MATHEMATICAL optimization , *HERBAL medicine , *NEURODEGENERATION , *DEMENTIA , *ACETYLCHOLINESTERASE , *BIOLOGICAL assay , *IMMUNOHISTOCHEMISTRY , *ALZHEIMER'S disease , *SYNAPSES - Abstract
Abstract: Optimized-SopungSunkiwon (OSS) is a multi-herbal formula that contains six medicinal herbs from SopungSunkiwon, a traditional medicine used for neurodegenerative disorders. In this study, we investigated the anti-amnesic effects of OSS in a dementia model. Acetylcholinesterase (AChE) inhibition assay was performed to investigate the cholinergic antagonistic effect of OSS. In addition, a step-through passive-avoidance test was performed with scopolamine-induced memory impairment in mice, and immunohistochemistry was analyzed to investigate synaptic formation with synaptic proteins. OSS inhibited AChE activity, resulting in significant improvement of memory functions. In the passive-avoidance test, the latency time of OSS-treated mice was significantly longer than that of either the control or scopolamine-treated group. In the immunohistochemical analysis, synaptic proteins such as synaptophysin and PSD-95 were significantly increased in OSS-treated mice. These results demonstrate that OSS may affect impairment and enhancement of memory and increase synaptophysin and PSD-95 facilitating acetylcholine release and synaptic growth. [Copyright &y& Elsevier]
- Published
- 2011
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14. Cuscutae Japonicae Semen Ameliorates Memory Dysfunction by Rescuing Synaptic Damage in Alzheimer's Disease Models.
- Author
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Ju, In Gyoung, Kim, Namkwon, Choi, Jin Gyu, Lee, Jong Kil, and Oh, Myung Sook
- Abstract
Alzheimer's disease (AD) is the most common type of dementia in the elderly. It is characterized by the accumulation of amyloid-beta (Aβ) and progressive cognitive impairment. To alleviate the symptoms of AD, functional foods and nutrients have been used for centuries. In this study, we investigated whether Cuscutae Japonicae Semen (CJS), a medicinal food traditionally used in East Asia, has effects on memory improvement and synapse protection in AD. We orally administered CJS to 5x familiar AD (5xFAD) transgenic mice and performed the Morris water maze test. The results showed that CJS treatment ameliorated the decline of memory function. Then, we demonstrated that CJS attenuated the degeneration of pre- and post-synaptic proteins in the hippocampi of 5xFAD mice. To demonstrate the effects of CJS in vitro, we treated Aβ in primary neuronal culture with CJS and observed that CJS rescued the loss of functional synapses. The protective effects of CJS on the synapse were due to the inhibition of activated caspase-3 expression. Additionally, CJS inhibited the phosphorylation of glycogen synthase kinase-3β and tau proteins, which contribute to synaptic dysfunction. Taken together, our results suggest that CJS is efficient in alleviating memory loss by rescuing caspase-3-mediated synaptic damage in AD treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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15. Butterbur Leaves Attenuate Memory Impairment and Neuronal Cell Damage in Amyloid Beta-Induced Alzheimer’s Disease Models.
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Kim, Namkwon, Choi, Jin Gyu, Park, Sangsu, Lee, Jong Kil, and Oh, Myung Sook
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ALZHEIMER'S disease , *NEURODEGENERATION , *AMYLOID beta-protein , *OXIDATIVE stress , *CELL death - Abstract
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease, and is characterized by the accumulation of amyloid beta (Aβ) as a pathological hallmark. Aβ plays a central role in neuronal degeneration and synaptic dysfunction through the generation of excessive oxidative stress. In the present study, we explored whether leaves of
Petasites japonicus (Siebold & Zucc.) Maxim. (PL), called butterbur and traditionally used in folk medicine, show neuroprotective action against Aβ25–35 plaque neurotoxicity in vitro and in vivo. We found that PL protected Aβ25–35 plaque-induced neuronal cell death and intracellular reactive oxygen species generation in HT22 cells by elevating expression levels of phosphorylated cyclic AMP response element-binding protein, heme oxygenase-1, and NAD(P)H quinine dehydrogenase 1. These neuroprotective effects of PL were also observed in Aβ25–35 plaque-injected AD mouse models. Moreover, administration of PL diminished Aβ25–35 plaque-induced synaptic dysfunction and memory impairment in mice. These findings lead us to suggest that PL can protect neurons against Aβ25–35 plaque-induced neurotoxicity and thus may be a potential candidate to regulate the progression of AD. [ABSTRACT FROM AUTHOR]- Published
- 2018
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16. 6-Shogaol, an active constituent of ginger, attenuates neuroinflammation and cognitive deficits in animal models of dementia.
- Author
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Moon, Minho, Kim, Hyo Geun, Choi, Jin Gyu, Oh, Hyein, Lee, Paula KJ, Ha, Sang Keun, Kim, Sun Yeou, Park, Yongkon, Huh, Youngbuhm, and Oh, Myung Sook
- Subjects
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SHOGAOL , *GINGER , *COGNITIVE ability , *DEMENTIA , *DRUG administration , *ANIMAL models in research - Abstract
Highlights: [•] 6-Shogaol resulted in amelioration of gliosis in intrahippocampal AβO-injected mice. [•] Memory impairment was alleviated by 6-shogaol administration in mouse model of AD. [•] 6-Shogaol ameliorated memory loss in scopolamine model of dementia. [•] 6-Shogaol enhanced the cognitive function under normal condition. [•] 6-Shogaol induced NGF up-regulation and synaptogenesis. [Copyright &y& Elsevier]
- Published
- 2014
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17. Protective effects of CCL01 against Aβ-induced neurotoxicity in 5xFAD transgenic mouse model of Alzheimer's disease.
- Author
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Ju, In Gyoung, Son, Su Young, Lee, Seungmin, Im, Hyeri, Huh, Eugene, Eo, Hyeyoon, Choi, Jin Gyu, Sohn, Mi Won, Yim, Sung-Vin, Kim, Sun Yeou, Kim, Dong-Hyun, Lee, Choong Hwan, and Oh, Myung Sook
- Subjects
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ALZHEIMER'S disease , *TRANSGENIC mice , *LABORATORY mice , *MITOGEN-activated protein kinases , *ANIMAL disease models , *CHRONIC traumatic encephalopathy - Abstract
Alzheimer's disease (AD) is the most common dementia characterized by the excessive accumulation of amyloid-beta (Aβ) and tau aggregates, as well as neuronal damage and neuroinflammation. Metabolic disruption in AD has been noticed because metabolite alterations closely correlate with Aβ neuropathology and behavioral phenotypes. Accordingly, controlling various neuropathological processes and metabolic disruption is an efficient therapeutic strategy for AD treatment. In this study, we evaluated the effects of a combination of Cuscuta seeds and Lactobacillus paracasei NK112 (CCL01) on AD neuropathology and altered metabolism in five familial AD (5xFAD) transgenic mice and neuronal cell cultures. First, we observed that CCL01 exerted neuroprotective effects in HT22 hippocampal neurons and primary cultured neurons. CCL01 ameliorated memory decline and protected synapses and neuronal survival in 5xFAD mice. These effects were related to the inhibition of tau phosphorylation. CCL01 also inhibited the activation of mitogen-activated protein kinase (MAPK) signaling and neuroinflammatory processes. Moreover, the metabolite profile—particularly characterized by altered phospholipid metabolism—was significantly changed in the 5xFAD group, while CCL01 partly restored the alteration. Lysophosphatidylcholine (lysoPC), the levels of which were higher in the brains of 5xFAD mice, exerted neurotoxicity in vitro, whereas CCL01 protected neurons from lysoPC-induced toxicity by regulating MAPK signaling. Additionally, CCL01 administration reduced gut inflammation in the 5xFAD mice. In summary, we demonstrated that CCL01 improved the memory function of 5xFAD mice by protecting neurons against Aβ- and lysoPC-induced toxicity through the regulation of MAPK signaling, neuroinflammation, tau phosphorylation, and gut inflammation, suggesting the potential of CCL01 as treatment for AD. [Display omitted] • CCL01 ameliorated memory decline and protected synapses and neuronal survival. • CCL01 inhibited tau phosphorylation, p38 MAPK activation, and neuroinflammation. • Untargeted metabolomics revealed that CCL01 modulated phospholipid metabolism. • CCL01 protected neurons against lipid metabolite-induced toxicity. • CCL01 inhibited gut inflammation. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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