• The Journal of Internal Korean Medicine
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• v.22 no.3
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• pp.331-339
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• 2001

목적 : 본 연구는 식풍해경(熄風解痙), 소산풍열(疏散風熱) 효능이 있는 백강잠이 치매에 미치는 영향을 알아보기 위하여 실험을 행하였다. 방법 : 치매 유발물질인 $amyloid{\beta}(A{\beta})$ 25-35를 흰쥐의 뇌 astrocyte에 처리한 후 대표적인 항산화 효소인 catalase, superoxide dismutase,glutathione peroxidase 및 glutathione-S-transferase의 활성 변화와 NO 생성 변화를 관찰하였다. 결과 $A{\beta}$ 25-35 처리로 catalase와 superoxide dismutase 활성이 현저히 감소하였으나 백강잠을 처리한 경우는 이들 효소 활성이 크게 증가하였다. 그리고, $A{\beta}$ 25-35의 농도에 의존적으로 증가된 NO 생성은 백강잠의 농도에 의존적으로 유의성 있게 억제되는 것으로 나타났다. 결론 : 백강잠은 항산화계 효소의 활성화 및 $A{\beta}$처리와 같은 치매유발 물질의 독성에 대한 적응능력 향상을 통하여 astrocyte를 보호하는 효능을 가지는 것으로 사료되며, 아울러 노인성 치매 등 임상적 응용에 그 효과가 기대된다.

• Journal of Oriental Neuropsychiatry
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• v.19 no.1
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• pp.29-42
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• 2008

Objectives : This study was performed to examine the effect of Sinchim on enhancing of memory in rat with water maze. Methods : Experimental animals(white rat) were classfied into normal, control, and aroma sample group. Then, they were injected .{\beta}-amyloid into control and aroma sample group rat's brain about $5{\mu}l$ to injure its brain. After rat smelt Sinchim about 12days, I did water maze test and anatomized its hippocampus. Sections were cut coronally at 30 ${\mu}m$.(XI00) Results: 1. In acquisition test of water maze learning, .{\beta}-amyloid injured group took more time than normal group to reach the escape platform noticeably and through the session of trial, Sinchim aroma sample group shortened time than .l3-amyloid injured group after 6 days. 2. In the acetyltransferase(AchE) immunostained method, it was shown that Sinchim aroma sample recovered tbe syntbesis of ChAT(Choloneacetyltransferase). Conclusion: Smelling Sinchim would be useful for enhancing of memory.

• Animal cells and systems
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• v.5 no.2
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• pp.139-143
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• 2001

Alzheimer's disease is the most common form of dementia and no cure is known so far. Extensive genetic works and in vitro experiments combined with clinical observations link amyloid $\beta$--protein (A$\beta$-) to the pathogenesis of Alzheimer's disease (AD). It was hypothesized that $A\beta$- becomes toxic when it adopts a fibrillar conformation. Recently, non-fibrillar form of $A\beta$- was observed and the potential role in the pathogenesis of AD became an interesting subject. In this study, the cytotoxicity of non-fibrillar $A\beta$- and fibrillar $A\beta$- was compared on oxidative stress, membrane damage, or nucleosome break down. Non-fibrillar $A\beta$- was not toxic in peripheral nervous system-derived cells but significantly toxic in central nervous system-derived cells while fibrillar $A\beta$- was non-selectively toxic in both cell culture. The neurotoxicity of non-fibrillar $A\beta$- was reproduced in semi-in vivo culture of mouse brain slice. In conclusion, non-fibrillar $A\beta$- could be more relevant to the selective neurodegeneration in Alzheimer's brains than fibrillar $A\beta$- and further research needs to be done for identification of the cause of AD.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.408-415
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• 2023

Alzheimer's disease constitutes a large proportion of all neurodegenerative diseases and is mainly caused by excess aggregation of amyloid beta (Aβ), which results in oxidative stress, inflammation, and apoptosis in the neurons. Populus tomentiglandulosa belongs to the Salicaceae family and is widely distributed in Korea; the antioxidant activities of the extract and fractions from P. tomentiglandulosa have been demonstrated in previous studies. Specifically, the ethyl acetate (EtOAc) fraction of P. tomentiglandulosa (EtOAc-PT) shows the most powerful antioxidative activity. Therefore, the present study investigates the protective effects of EtOAc-PT against neuronal damage in Aβ_25-35-stimulated SH-SY5Y cells. EtOAc-PT restored cell viability significantly as well as inhibited the levels of reactive oxygen species and lactate dehydrogenase release compared to the Aβ_25-35-induced control group. Furthermore, the inflammation- and apoptosis-related protein expressions were investigated to demonstrate its neuroprotective mechanism. EtOAc-PT downmodulated the expressions of inducible nitric oxide synthase, cyclooxygenase-2, B-cell lymphoma 2 associated X, and B-cell lymphoma 2. Thus, the findings show that EtOAc-PT has protective effects against Aβ_25-35 by suppressing oxidative stress, inflammation, and apoptosis.

• Journal of the Korean Society of Radiology
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• v.83 no.3
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• pp.453-472
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• 2022

Over the past decades, the immense clinical need for early detection methods and treatments for dementia has become a priority worldwide. The advances in PET biomarkers play increasingly important roles in understanding disease mechanisms by demonstrating the protein pathology underlying dementia in the brain. Amyloid-β and tau deposition in PET images are now key diagnostic biomarkers for the Alzheimer's disease continuum. The inclusion of biomarkers in the diagnostic criteria has achieved a paradigm shift in facilitating early differential diagnosis, predicting disease prognosis, and influencing clinical management. Furthermore, in vivo images showing pathology could become prognostic as well as surrogate biomarkers in therapeutic trials. In this review, we focus on recent developments in radiotracers for amyloid-β and tau PET imaging in Alzheimer's disease and other neurodegenerative diseases. Further, we introduce their potential application as future perspectives.

• Molecular & Cellular Toxicology
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• v.4 no.2
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• pp.157-163
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• 2008

Formation of ${\beta}$-amyloid $(A{\beta})$ fibrils has been identified as one of the major characteristics of Alzheimer's disease (AD). Inhibition of $A{\beta}$ fibril formation in the CNS would be attractive therapeutic targets for the treatment of AD. Several small compounds that inhibit amyloid formation or amyloid neurotoxicity in vitro have been known. Citrate has surfactant function effect because of its molecular structure having high anionic charge density, in addition to the well-known antibacterial and antioxidant properties. Therefore, we hypothesized that citrate might have the inhibitory effect against $A{\beta}$ fibril formation in vitro and have the protective effect against $A{\beta}$-induced neurotoxicity in PC12 cells. We examined the effect of citrate against the formation of $A{\beta}$ fibrils by measuring the intensity of fluorescence in thioflavin-T (Th-T) assay of between $A{\beta}_{25-35}$ groups treated with citrate and the control with $A{\beta}_{25-35}$ alone. The neuroprotective effect of citrate against $A{\beta}$-induced toxicity in PC12 cells was investigated using the WST-1 assay. Fluorescence spectroscopy showed that citrate inhibited dose-dependently the formation of $A{\beta}$ fibrils from ${\beta}$-amyloid peptides. The inhibition percentages of $A{\beta}$ fibril formation by citrate (1, 2.5, and 5 mM) were 31%, 60%, and 68% at 7 days, respectively in thioflavin-T (Th-T) assay. WST-1 assay revealed that the toxic effect of $A{\beta}_{25-35}$ was reduced, in a dose-dependent manner to citrate. The percentages of neuroprotection by citrate (1, 2.5, and 5 mM) against $A{\beta}-induced$ toxicity were 19%, 31 %, and 34%, respectively. We report that citrate inhibits the formation of $A{\beta}$ fibrils in vitro and has neuroprotective effect against $A{\beta}$-induced toxicity in PC12 cells. Neuroprotective effects of citrate against $A{\beta}$ might be, to some extent, attributable to its inhibition of $A{\beta}$ fibril formation. Although the mechanism of anti-amyloidogenic activity is not clear, the possible mechanism is that citrate might have two effects, salting-in and surfactant effects. These results suggest that citrate could be of potential therapeutic value in Alzheimer's disease.

• Journal of Sasang Constitutional Medicine
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• v.21 no.3
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• pp.138-153
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• 2009

1. Objectives: Yeolda-Hanso tang (YH) has long been used as traditional herbal formula in Korea as various diseases. Now we modified Yeolda-Hanso tang (YH) for neurodegenerative diseases treatment and named New-Yeolda-Hanso tang (NYH). We investigated neuroprotective effects of NYH on NGF-differentiated PC12 cells cytotoxicity induced by $\beta$-Amyloid peptide (A$\beta$25-35) and evaluated the ability of NYH to prevent and treat for neurodegenerative diseases via autophagy enhancement. 2. Methods and Results: 1) Protective effect of NYH on PC12 cells cytotoxity induced by A$\beta$25-35. PC12 cells survival was measured by MTT and lactate dehydrogenase (LDH) assay. $20{\mu}M$ $\beta$-Amyloid peptide (A$\beta$25-35) induced cytotoxicity on NGF-differentiated PC12 cells. NYH attenuated the cytotoxic effects of A$\beta$25-35 in a dose-dependent manner. 2) Pharmacological induction of Autophagy by NYH in PC12 cells Autophagy induction and activation was measured by immunoblot assay. Marker of autophagy, LC3 II expression and the ratio of LC3-II/I was slightly increased in the protein treated with YH, and significantly augmented in the protein treated with NYH. NYH-induced increase of LC3-II protein level was inhibited by 3MA. 3) Induction of Autophagy by NYH on A$\beta$25-35-induced injury in PC12 cells In MTT assay, $100{\mu}g/ml$ re-treated NYH attenuated $20{\mu}M$ A$\beta$25-35-induced cytotoxicity in PC12 cells. Protection effect of NYH was blocked by autophagy inhibitor 3MA. In immunoblot assay, $1200{\mu}g/ml$ pre-treated NYH activated autophagy in $20{\mu}M$ A$\beta$25-35-induced cytotoxicity in PC12 cells. The observed effect was partially blocked by 3MA. 3. Conclusions: All the results indicated that NYH possesses neuroprotective potential partially mediated by autophagy enhancement and NYH may be considered to be a promising new herbal formula to prevent and treat for neurodegenerative diseases including Alzheimer's disease (AD).

• Journal of the Korean Applied Science and Technology
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• v.35 no.2
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• pp.389-398
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• 2018

This study was to investigate the antioxidant and anti-amyloid activities of the extract (KP-HE) from Kalopanax pictus (KP) fermented with Hericium erinaceum (HE) mycelium. Antioxidant activity was evaluated based on 2,2-diphenyl-1-picrylhydrazyl radical (DPPH) and 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) radical(ABTS) scavenging assays. In all assays, the extracts from KP, HE and KP-HE had the potential for antioxidant activities. However, antioxidant activity of KP-HE significantly scavenged DPPH radical as compared to the KP and HE. The result suggested that the antioxidant component was increased in the process of KP fermented with HE. KP-HE was shown to significantly inhibite peroxyl radical-mediated DNA strand breakage whereas KP and HE did not inhibit DNA strand breakage. The aggregation of the amyloid-${\beta}$ ($A{\beta}$) peptide is involved in the pathological process of Alzheimer's disease(AD). In this study, the effects of KP, HE and KP-HE on the aggregation of $A{\beta}_{1-42}$ were investigated. KP and HE had little effect on $A{\beta}$ aggregation and KP-HE effectively inhibited $A{\beta}$ aggregation. KP-HE effectively inhibited $A{\beta}$ induced cell death and significantly increased of the 20.3% cell survival at $300{\mu}g/mL$ concentration. KP-HE also decreased intracellular reactive oxygen specie levels in $A{\beta}$-treated cells. The results suggested that KP-HE had antioxidant and anti-amyloid activities. Therefore, KP-HE could potentially be used as a valuable functional food ingredient to prevent neurodegenerative disorders such as AD.

• Korean Journal of Food Science and Technology
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• v.36 no.6
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• pp.1026-1031
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• 2004

Acetylcholinesterase inhibitory activity and protective effect against cytotoxicity of PC 12 cell induced by beta-amyloid protein and glutamate were examined in perilla seed methanol extract and its solvent fractions. Methanol extract of perilla seed showed dose-dependent acetylcholinesterase inhibitory activity, with n-butanol fraction showing strongest activity. Perilla seed methanol extract also decreased glutamate- and ${\beta}-amyloid$ protein $(A{\beta})-induced$ cytotoxicities of PC 12 cells dose-dependently. Formation of TBARS induced by $FeSO_{4^-}H_2O_2$ in rat brain was significantly reduced by perilla seed methanol extract, with strongest protective activity formation of TBARS shown in n-butanol fraction. Results suggest perilla seed methanol extract may attenuate actylcholinesterase activity and cytotoxicity induced by glutamate and ${\beta}-amyloid$ protein through suppression of oxidative stress.

• Food Science and Preservation
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• v.14 no.4
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• pp.425-430
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• 2007

To investigate the potential therapeutic value of a plant extract against amyloid ${\beta}-peptide-induced$ cell damage, we first screened extracts of 250 herbs, and finally selected a water extract of Spinacia oleracea for further study. This extractshowed the potential to inhibit the reactions of oxidants. We measured the angiotensin-converting-enzyme (ACE) inhibitory activity of the extract, and assessed the ability of the extract to protect neuronal cells from chemical-induced cell death. SH-SY5Y neuroblastoma cells were used in this assay. The extract exerted protective effects on $H_2O_2-induced$ cell death, when $H_2O_2$ was used at 100 M, 200 M, and 500 M (protection of 87%, 73%, and 58%, respectively). When 50 M of amyloid ${\beta}-peptide$ was added to the test cells, however, the extract had no protective effect on cell death. The extract inhibited ACE activity in a dose-dependent manner, and exhibited potent protection against the deleterious effects of $H_2O_2$. In sum, these results suggest that a water extract of Spinacia oleracea has the potential to afford protection against chemical-induced neuronal cell death, and the extract may be useful in the treatment of neurodegenerative diseases. The precise molecular mechanism of neuroprotection is under investigation.