• IMMUNE NETWORK
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• 제5권4호
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• pp.252-257
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• 2005

Background: This study was designed to investigate the effect of exercise training on defense mechanism of chronic degenerative disease, aging, and memory impairments of senescence-accelerated mouse (SAM)P8 under the hypothesis that "Senile dementia may be prevented by regular exercises". Methods: To evaluate the effects of exercise training on the defense mechanism of aging and memory impairment, SAMP8 were divided into two groups, the control group and exercise training groups. the exercise training group were performed with low $(\dot{V}O_2max\;25{\sim}33%)$, middle ($\dot{V}O_2max$ 50%) and high $(\dot{V}O_2max\;66{\sim}75%)$ intensity exercise. All SAMP8 mice were fed experimental diet ad libitum until 4, 8 months, and dead period. Results: Median lifespan in middle exercise group resulted in a significantly increased (23.5% and 18.7%, respectively), whereas these lifespan in high exercise group resulted in an unexpectedly decreased (13.5% and 12.1%, respectively) compared with control group. Body fat levels in 4 and 8 months of age were significantly decreased 43% to 51% in middle exercise group, whereas were remarkably deceased to 57% in high exercise group compared with control group. It is believed that extended median and maximum lifespan may be effected by calory restriction through the exercise training. Acetylcholine (ACh) levels were significantly increased 6.7% and 8.5% in middle and high exercise groups, and also choline acetyltransfease (ChAT) activities were significantly increased 10.3% and 11.9% in middle and high exercise groups. Conclusion: These results suggest that proper and regular exercises such as middle group ($\dot{V}O_2max$ 50%) may play an effective role in attenuating an oxygen radicals and may play an important role in improving a learning and memory impairments of senile dementia.

• 동의신경정신과학회지
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• 제20권2호
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• pp.1-17
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• 2009

Objectives : Alzheimer's disease(AD) is the most common form of dementia, which is characterized by progressive deterioration of memory and higher cortical functions that ultimately results in total degradation of intellectual and mental activities. Nokyongdaebo-tang(Lurongdabutang) has been usually used for the treatment for the deficiency syndrome dementia and amnesia. This experiment was designed to investigate the effect of the Nokyongdaebo-tang(Lurongdabutang) hot water extract on pathological AD model. Methods : The effects of the Nokyongdaebo-tang(Lurongdabutang) hot water extract on cultured spinal cord cells induced by ${\beta}$-amyloid were investigated. The effects of the Nokyongdaebo-tan(Lurongdabutang) hot water extract on the memory deficit mice induced by scopolamine were investigated. Results : 1. ${\beta}$-amyloid treatment on cultured spinal cord cells increased both GFAP-staining intensity of astrocytes and caspase 3 immunoreactivity on cultured cells. Then, Nokyongdaebo-tang(Lurongdabutang) treatment reduced the labeling intensity for both GFAP and caspase 3 proteins in culture cells. 2. Scopolamine treatment into mice increased levels of GFAP-positive astrocytes and caspase 3-labeled cells of the hippocampal subfields dentate hilar region, CA3 and CA1 area. In vivo administration of Nokyongdaebo-tang(Lurongdabutang) attenuated labeling intensity for those two proteins in the same hippocampal areas. Similar effects were observed by the treatment of galanthamine, an inhibitor of acetylcholinesterase. Conclusions : This experiment shows that the Nokyongdaebo-tang(Lurongdabutang) may play a protective role in damaged neural tissues. Since neuronal damage seen in degenerative brains such as AD are largely unknown, the current data may provide possible insight into therapeutic strategies for AD treatments. Nokyongdaebo-tang(Lurongdabutang) might be effective for the prevention and treatment of AD.

• 통합자연과학논문집
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• 제16권2호
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• pp.61-67
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• 2023

Human body ages differently due to environmental, genetic and pathological factors. DNA methylation patterns also differs depending on various factors such as aging and several other diseases. The aging clock model, which uses these differences to predict age, analyzes DNA methylation patterns, recognizes age-specific patterns, predicts age, and grasps the speed and degree of aging. Aging occurs in everyone and causes various problems such as deterioration of physical ability and complications. Alzheimer's disease is a disease associated with aging and the most common brain degenerative disease. This disease causes various cognitive functions disabilities such as dementia and impaired judgment to motor functions, making daily life impossible. It has been reported that the incidence and progression of this disease increase with aging, and that increased phosphorylation of Aβ and tau proteins, which are overexpressed in this disease and accelerates epigenetic aging. It has also been reported that DNA methylation is significantly increased in the hippocampus and entorhinal cortex of Alzheimer's disease patients. Therefore, we calculated the biological age using the Epi clock, a pan-tissue aging clock model, and confirmed that the epigenetic age of patients suffering from Alzheimer's disease is lower than their actual age. Also, it was confirmed to slow down aging.

• 동의신경정신과학회지
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• 제10권1호
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• pp.53-78
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• 1999

As the average life span have been lengthened and the rate of senile population have been raised, chronic degenerative diseases incident to aging has been increased rapidly and become a social problem. With this social background, recently, the facts that oxygen radicals(OR) have toxic effects on Central Nervous System and Peripheral Nervous System and cause neuropathy such as Parkinson's Disease, Alzheimer Disease have been turned out, and accordingly lots of studies on the mechanism of the toxic effects of OR on nerves, the diseases caused by OR and the approaches to curing the diseases have been made. The purpose of this study is to examine the toxic effects caused by Glucose Oxidase(GO) and the effects of herbal extracts such as Chilbokyeum(CBY), Chilbokyeumga Acori Rhizoma(CAR), Acori Rhizoma(AR) on the treatment of the toxic effects. For this purpose, experiments with the cultured cell from the cerebrums of new born mice were done. The results of these experiments were as follows. 1. GO, a oxygen radical, decreased the survival rate of the cultured cells on NR assay, MTT assay and amount of neurofilaments and increased the amount of total protein, lipid peroxidation and the amount of LDH. 2. CBY have efficacy of increasing the amount of neurofilaments and total protein and decreasing lipid peroxidation and the amount of LDH. 3. CAR have efficacy of increasing the amount of neurofilaments and total protein and decreasing lipid peroxidation and the amount of LDH. 4. AR have efficacy of increasing the amount of neurofilaments and total protein. From the above results, It is concluded that Chilbokyeumgamibang has marked efficacy as a treatment for the damages caused in the GO-mediated oxidative process. And Chilbokyeumgamibang is thought to have certain pharmacological effects on controlling over aging and treating Dementia. Further clinical study of this pharmacological effects of Chilbokyeumgamibang should be complemented.

• 한국방사선학회논문지
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• 제10권5호
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• pp.307-312
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• 2016

알츠하이머병은 치매를 일으키는 가장 흔한 퇴행성 뇌 질환이다. 뇌에 축적되는 베타 아밀로이드 단백질은 기억력감퇴, 언어능력 저하등 일상생활 수행 능력이 어렵게 된다. 베타 아밀로이드 플라그 농도는 인지장애를 가진 성인환자에서 알츠하이머 질환과 인지장애의 다른 원인인지를 평가하는 데 사용된다. 베타아밀로이드 단백질에 대한 높은 민감성과 특이성을 가진 $^{18}F$-Florbetaben을 이용하여 알츠하이머병을 조기진단에 유용성을 알아보고자 한다. $^{18}F$-FDG Brain 영상에서 특이소견 없음을 보인다. 그리고 MR-Brain 영상에서 해마의 위축이 없는 것으로 보였다. 하지만 $^{18}F$-Florobetaben에서 베타 아밀로이드의 섭취는 알츠하이머병의 진전이 되고 있음을 알려준다. 따라서, $^{18}F$-Florobetaben은 알츠하이머병을 조기 진단하는 데 매우 유용하다.

• 대한한의학회지
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• 제26권3호
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• pp.135-145
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• 2005

Objectives : This study investigated effect of Evodiae fructus water extract (EVOR) on apoptotic cell death induced by NaCN in SK-N-SH neuroblastoma cell lines. NaCN stimulates glutamate release which can activate glutamate receptors to initiate excitotoxic processes. This study examines the role of EVOR in mediating NaCN-induced cytotoxicity. Methods & Results : Cytotoxicity was assessed by measuring lactate dehydrogenase (LDH) in the culture media. NaCN(0.1mM) produced cytotoxicity following 12hrs of incubation. NaCN-induced cytotoxicity was partially blocked by EVOR. The treatment of EVOR in simultaneous exposure of cultures to NaCN provided complete protection against cytotoxicity. NaCN-induced cytotoxicity was found to inhibit DNA fragmentation, repaired by cell cycle and simultaneous exposure to NaCN, regenerated with neurite outgrowh by EVOR. These results indicate thaf damage by NaCN in neumnal cell cultures was repaired by EVOR, whereas NaCN-induced cytotoxicity is blocked Primarily by activation of anti-apoptosis. Conclusions : These results suggest that EVOR may be beneficial for the treatment of dementia and other degenerative problems of the central nervous system.

• EDISON SW 활용 경진대회 논문집
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• 제4회(2015년)
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• pp.14-23
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• 2015

Alzheimer's disease is one of the most common types of degenerative dementia. As a considerable cause of Alzheimer's disease, neurotoxic plaques composed of 39 to 42 residue-long amyloid beta($A{\beta}$) fibrils have been found in the patient's brain in large quantity. A previous study found that erythrosine B (ER), a red color food dye approved by FDA, inhibits the formation of amyloid beta fibril structures. Here, in an attempt to elucidate the inhibition mechanism, we performed molecular dynamics simulations to demonstrate the conformational change of $A{\beta}40$ induced by 2 ERs in atomistic detail. During the simulation, the ERs bound to the surfaces of both N-terminus and C-terminus regions of $A{\beta}40$ rapidly. The observed stacking of the ERs and the aromatic side chains near the N-terminus region suggests a possible inhibition mechanism in which disturbing the inter-chain stacking of PHEs destabilizes beta-sheet enriched in amyloid beta fibrils. The bound ERs block water molecules and thereby help stabilizing alpha helical structure at the main chain of C-terminus and interrupt the formation of the salt-bridge ASP23-LYS28 at the same time. Our findings can help better understanding of the current and upcoming treatment studies for Alzheimer's disease by suggesting inhibition mechanism of ER on the conformational transition of $A{\beta}40$ at the molecular level.

• 정신신체의학
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• 제29권1호
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• pp.67-76
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• 2021

연구목적 본 연구는 알츠하이머병 및 경도인지장애 환자에서 뇌의 퇴행성 변화 (내측두엽 위축, 대뇌백질병변) 및 신경인지기능과 일상생활 수행능력과의 연관성을 살펴보고자 하였다. 방 법 본 연구는 단면 연구로서, 알츠하이머병 및 경도인지장애로 진단받은 111명을 대상으로 하였다. 내측두엽 위축은 표준화된 시각 기반 척도(Scheltens scale)에 의해 평가하였으며, 대상군을 두 그룹으로 분류하였다. 일상생활 수행능력은 한국어판 블레스트 치매 척도-일상생활 수행능력(Korean version of Blessed Dementia Scale-Activity of daily living, BDS-ADL)으로 평가하였으며 신경인지기능은 The Korean version of the consortium to establish a registry for Alzheimer's disease (CERAD-K)로 평가하였다. 내측두엽 위축의 정도에 따른 일상생활 수행능력의 차이를 보기 위해 독립표본 t-test를 시행하였으며, 일상생활 수행능력과 신경인지기능과의 상관관계를 분석하기 위해 피어슨 상관분석 및 계층적 다중회귀분석을 시행하였다. 결 과 내측두엽 위축이 심할수록, 그리고 단어목록재인 검사 점수가 낮을수록 BDS-ADL 점수가 높았다(p<0.05). 계층적 다중회귀분석 결과 MMSE-K, 단어목록 재인검사 점수가 BDS-ADL의 유의한 예측인자로 나타났다(Adjusted R²=0.442, F=44.611, p<0.001). 결 론 알츠하이머병과 경도인지장애 환자에서 일상생활 수행능력은 내측두엽 위축 및 단어목록재인 검사 점수와 유의한 상관관계를 보였다. 일상생활 수행능력과 관련된 인자를 분석한 본 연구는 임상 실제에서 유용한 정보를 제공할 것으로 생각된다. 일상생활 수행능력과 뇌의 구조 및 기능과의 연관성에 대해서 추가적인 연구가 필요할 것으로 보인다.

• 생명과학회지
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• 제9권4호
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• pp.439-452
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• 1999

This study was designed to investigate the effects of sea tangle (Laminaria japonica) extract and fucoidan components on anti-aging action. Sprague-Dawley(SD) male rats (210$\pm$5g) were fed experimental diets Dasi-Ex group: sea tangle extract powder of 4.0% added to control diet; Fuco-I, II and III groups: funcoidan powder of 1, 2 and 3% added to Dasi-Ex group for 45 days. Hydroxyl radical (.OH) formations were significantly inhibited (10-20% and 25-30%) in serum and brain mitochondria of Dasi-Ex and Fuco-I, II and III groups compared with control group. Significant differences in .OH formations of brain mitochondria in Dasi-Ex and Fuco-I groups could not be obtained, but.OH formations of brain microsomes resulted in a significant decrease (15-20%) in Fuco-II and III groups compared with control group. Basal oxygen radical (BOR) formations were significantly decreased about 10% and 13-15% in brain mitochondria of Dasi-Ex and Fuco-I group, and Fuco-II, III groups, and also decreased about 10% and 15-20% in brain microsomes of Dasi-Ex and Fuco-I groups, and Fuco-II, III groups. LPO levels of brain mitochondria and microsomes were significantly inhibited about 10% in Dasi-Ex and Fuco-I, II groups and 15% in Fuco-III groups. Oxidized proteins (>C=O) were significantly inhibited about 10% in serum of Dasi-Ex and Fuco-I, II, III groups and brain mitochondria of Dasi-Ex group, while remarkably inhibited (30~35%) in brain mitochondria of Fuco-I, II and III groups. Nitric oxide (NO) levels were significantly inhibited (12~15%) in serum of Fuco-I, II and III groups, but there no significant difference in serum NO levels of Dasi-Ex group. Superoxide dismutase (SOD) activities were remarkably increased (30~ 60%) in serum of Fuco-I, II and III groups, but there were no significant differences in SOD activities in serum of Dasi-Ex group. Catalase (CAT) activities were significantly increased about 20% in serum of Dasi-Ex and Fuco-I, II, III groups. Mn-SOD activities in brain mitochondria were significantly increased about 17% in Dasi-Ex group, while remarkably increased 26~36% in Fuco-I, II, III groups. Cu,Zn-SOD activities in brain cytosol were dose-dependently of fucoidan increased 10%, 12% and 18%, respectively, compared with control group. These results suggest that anti-aging effects of fucoidan may play a pivotal role in attenuating a various age-related changes such as chronic degenerative disease and senile dementia.

• IMMUNE NETWORK
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• 제6권1호
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• pp.27-32
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• 2006

Background: Chronic inflammation in the brain has known to be associated with the development of a various neurological diseases including dementia. In general, the characteristic of neuro-inflammation is the activated microglia over the brain where the pathogenesis occurs. Pro-inflammatory repertoires, interleukin-1${\beta}$ (IL-1${\beta}$) and nitric oxide (NO), are the main causes of neuro-degenerative disease, particularly in Alzheimer's disease (AD) which is caused by neuronal destruction. Those pro-inflammatory repertoires may lead the brain to chronic inflammatory status, and thus we hypothesized that chronic inflammation would be inhibited when pro-inflammatory repertoires are to be well controlled by inactivating the signal transduction associated with inflammation. Methods: In the present study, we examined whether biphenyl dimethyl dicarboxylate (DDB), an active compound from Schizandra chinensis Baillon, inhibits the NO production by a direct method using Griess reagent and by RT-PCR in the gene expression of inducible nitric oxide synthase (iNOS) and IL-1${\beta}$. Western blots were also used for the analysis of NF-${\kappa}B$ and I${\kappa}B$. Results: In the study, we found that DDB effectively inhibited IL-1${\beta}$ as well as NO production in BV-2 microglial cell, and the translocation of NF-${\kappa}B$ was comparably inhibited in the presence of DDB comparing those to the positive control, lipopolysaccharide. Conclusion: The data suggested that the DDB from Schizandra chinensis Baillon may play an effective role in inhibiting the pro-inflammatory repertoires which may cause neurodegeneration and the results imply that the compound suppresses a cue signal of the microglial activation which can induce the brain pathogenesis such as Alzheimer's disease.