• 지역사회간호학회지
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• 제33권1호
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• pp.63-73
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• 2022

Purpose: The purpose of this study was to identify the predictors influencing fear of falling in community-dwelling elderly women with mild cognitive impairment (MCI). Methods: A secondary data analysis was performed using data of 65 years or older elderly women with MCI participating in the 7th Korea Longitudinal Study of Ageing of the Korea Employment Information Service. The study subjects included 368 elderly women with MCI. For data analysis, descriptive statistics and logistic regression with complex samples were performed using IBM SPSS ver. 23.0. Results: 89.9% of the elderly women with MCI had fear of falling. There were significant factors such as religion (OR=8.85, 95% CI: 3.39~23.15), restriction of activity (OR=6.84, 95% CI: 2.14~21.90), depression (OR=0.75, 95% CI: 0.62~0.90), and MMSE (OR=1.30, 95% CI: 1.03~1.63), predicting fear of falling in community-dwelling elderly women with MCI. Conclusion: Differentiated strategies should be developed for elderly women with MCI to decrease fear of falling and prevent falls with understanding of contributing factors. This study will provide fundamental information on programming and a policy proposal related to fear of falling for elderly women with MCI.

• 보건행정학회지
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• 제30권4호
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• pp.493-504
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• 2020

Background: There have been many studies on the associations between body mass index (BMI) and cognitive function. However, no study has ever compared the associations across the methods of categorizing BMI. In this study, we aimed to fill the gap in the previous studies and examine whether the obesity paradox is valid in the risk of cognitive function. Methods: Of the 10,254 people aged 45 and older from the Korean Longitudinal Study of Ageing from 2006 to 2016, 8,970 people were finalized as the study population. The dependent variable was whether a person has a normal cognitive function or not, and the independent variables of interest were BMI categorized by the World Health Organization Western Pacific Regional Office (WHO-WPRO) method, the WHO method, and a 10-group method. Covariates included sociodemographic factors, health behavior factors, and health status factors. A generalized linear mixed model analysis with a logit link was used. Results: In the adjusted model with all covariates, first, in the case of BMI categories of the WHO-WPRO method, underweight (odds ratio [OR], 1.16; 95% confidence interval [CI], 1.15-1.17), overweight (OR, 1.36; 95% CI, 1.35-1.36), and obese (OR, 1.34; 95% CI, 1.33-1.34) groups were more likely to have a normal cognitive function than a normal-weight group. Next, in the case of BMI categories of the WHO method, compared to a normal-weight group, underweight (OR, 1.15; 95% CI, 1.14-1.16) and overweight (OR, 1.06; 95% CI, 1.06-1.07) groups were more likely to have a normal cognitive function; however, obese (OR, 0.62; 95% CI, 0.61-0.63) group was less likely to have it. Lastly, in the case of the 10-group method, as BMI increased, the likelihood to have a normal cognitive function changed like a wave, reaching a global top at group-7 (26.5 kg/㎡ ≤ BMI <28.0 kg/㎡). Conclusion: The associations between BMI and cognitive function differed according to how BMI was categorized among people aged 45 and older in Korea, which suggests that cognitive function may be positively associated with BMI in some categories of BMI but negatively in its other categories. Health policies to reduce cognitive impairment need to consider this association between BMI and cognitive function.

• 한국약용작물학회:학술대회논문집
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• 한국약용작물학회 2011년도 추계학술발표회
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• pp.31-45
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• 2011

The amyloid ${\beta}$-peptide ($A{\beta}$), which originates from the proteolytic cleavage of amyloid precursor protein (APP), plays a central role in the pathogenesis of Alzheimer's disease (AD). Mounting evidence indicates that different species of $A{\beta}$, such as $A{\beta}$ oligomers and fibrils, may contribute to AD pathogenesis via distinct mechanisms at different stages of the disease. Importantly, elevation and accumulation of soluble $A{\beta}$ oligomers closely correlate with cognitive decline and/or disease progression in animal models of AD. In agreement with these studies, oligomers of $A{\beta}$ have been shown to directly affect synaptic plasticity, a neuronal process that is known to be essential for memory formation. Our previous studies showed that $A{\beta}$ induces the breakdown of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), a phospholipid that regulates key aspects of neuronal function. PI(4,5)P2 breakdown was found to be a key step toward synaptic and memory dysfunction in a mouse model of AD. To this end, we seek to identify small molecules that could elevate the levels of PI(4,5)P2 and subsequently block $A{\beta}$ oligomer-induced breakdown of PI(4,5)P2 and synaptic dysfunction.. We found that (20S)Rg3, an active triterpene glycoside from heat-processed ginseng, serves as an agonist for phosphatidylinositol 4-kinase IIalpha (PI4KIIalpha), which is a lipid kinase that mediates a rate-limiting step in PI(4,5)P2 synthesis. Consequently, (20S)Rg3 stimulates PI(4,5)P2 synthesis by directly stimulating the activity of PI4KIIalpha. Interestingly, treatment of a mouse model of AD with (20S)Rg3 leads to reversal of memory deficits. Our data suggest that the PI(4,5)P2-promoting effects of (20S)Rg3 may help mitigate the cognitive symptoms associated with AD.

• Parasites, Hosts and Diseases
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• 제55권3호
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• pp.267-285
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• 2017

Angiostrongylus cantonensis invades the central nervous system (CNS) of humans to induce eosinophilic meningitis and meningoencephalitis and leads to persistent headache, cognitive dysfunction, and ataxic gait. Infected mice (nonpermissive host), admittedly, suffer more serious pathological injuries than rats (permissive host). However, the pathological basis of these manifestations is incompletely elucidated. In this study, the behavioral test, histological and immunohistochemical techniques, and analysis of apoptotic gene expression, especially caspase-3, were conducted. The movement and motor coordination were investigated at week 2 post infection (PI) and week 3 PI in mice and rats, respectively. The cognitive impairs could be found in mice at week 2 PI but not in rats. The plaque-like lesion, perivascular cuffing of inflammatory cells, and dilated vessels within the cerebral cortex and hippocampus were more serious in mice than in rats at week 3 PI. Transcriptomic analysis showed activated extrinsic apoptotic pathway through increased expression of TNFR1 and caspase-8 in mice CNS. Immunohistochemical and double-labeling for NeuN and caspase-3 indicated the dramatically increased expression of caspase-3 in neuron of the cerebral cortex and hippocampus in mice but not in rats. Furthermore, western-blotting results showed high expression of cleaved caspase-3 proteins in mice but relatively low expression in rats. Thus, extrinsic apoptotic pathway participated in neuronal apoptosis might be the pathological basis of distinct behavioral dysfunctions in rodents with A. cantonensis infection. It provides the evidences of a primary molecular mechanism for the behavioral dysfunction and paves the ways to clinical diagnosis and therapy for A. cantonensis infection.

• 생물정신의학
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• 제9권2호
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• pp.103-111
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• 2002

Neurocognitive research focusing on cognitive deficits in Depression has resulted in several important but yet potentially contradictory findings. Much literature documents the presence of significant neurocognitive impairments in depressive patients. Studies have shown that dysthymic disorder patients demonstrate a diffuse pattern of cognitive impairment which is frequently indistinguishable from that of focal braindamaged patients. Some reports have suggested that there is a focal pattern of deficit, such as anterior cingulate dysfunction, frontal lobe impairment, or dysfunction of the temporal-limbic cortex. The aim of this study is to evaluate the neurocognitive functions in dysthymic disorder patients, and to compare the functions with those of major depressive disorder patients. The subjects are 17 dysthymic disorder patients. And their neurocognitive functions are compared with those of 23 major depressive episode patients. Patients with a history of neurologic disease, alcohol dependence, substance abuse and mental retardation are excluded. They are assessed with a part of Vienna Test System which is computerized neurocognitive function tests and can evaluate attention, eductive ability, reproductive ability, visuoperceptual analysis, vigilance, visual immediate memory, the speed of information-processing, judgement, and fine motor coordinations. There are no other specific difference between two groups, except the result of cognitrone test. This study provides information about the neurocognitive functions and some difference between major depressive disorder patients and carefully diagnosed dysthymic disorder patients.

• 디지털융복합연구
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• 제18권9호
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• pp.249-256
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• 2020

본 연구의 목적은 노인의 거주형태에 따라 사망 위험요인에 차이가 있는지 파악하기 위함이다. 본 연구는 2014년도 고령화연구패널조사를 이차 분석한 연구로 노인 3,827명을 2년간 추적조사한 종단연구이다. 자료 분석을 위해 콕스 비례 위험 회귀 분석으로 분석하였다. 본 연구결과, 동거노인은 성별, 교육수준, 주관적 건강 상태, IADL 제한, 인지기능 장애, 우울 증상이 사망에 영향을 주는 요인이었으며, 독거노인은 규칙적 운동 여부, IADL 제한, 인지기능 장애가 사망에 영향을 주는 것으로 나타났다. 본 연구는 거주형태에 따라 사망 위험요인 간에 차이가 있는지 규명하였다는 점에서 의의가 있다. 본 연구 결과에 따라 노인의 거주형태에 따라 사망률을 줄이기 위한 간호 중재를 개발해야 할 것이다.

• 한국약용작물학회지
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• 제25권6호
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• pp.353-360
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• 2017

Background: A critical features of Alzheimer's disease (AD) is cognitive dysfunction, which partly arises from decreased in acetylcholine levels. AD afftected brains are characterized by extensive oxidative stress, which is thought to be primarily induced by the amyloid beta ($A{\beta}$) peptide. In a previous study, Cinnamomum loureiroi tincture inhibited acetylcholinesterase (AchE) activity. That study identified AChE inhibitor in the C. loureiroi extract. Furthermore, the C. loureiroi extract enhanced memory in a trimethyltin (TMT)-induced model of cognitive dysfunction, as assessed via two behavioral tests. Rosa laevigata extract protected against oxidative stress-induced cytotoxicity. Administrating R. laevigata extracts to mice significantly reversed $A{\beta}$-induced learning and memory impairment, as shown in behavioral tests. Methods and Results: We conducted behavioral to examine the synergistic effects of C. loureiroi and R. laevigata extracts in inhibiting AChE and counteracting TMT-induced learning and memory losses. We also performed biochemical assays. The biochemical results showed a relationship between increased oxidative stress and cholinergic neurons damage in TMT-treated mice. Conclusions: A diet containing C. loureiroi and R. laevigata extracts ameliorated learning and memory impairments in the Y-maze and passive avoidance tests, and exerted synergistic inhibitory effect against AChE and lipid peroxidation.

• 동의생리병리학회지
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• 제23권5호
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• pp.1080-1086
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• 2009

This study was designed to investigate the effects of Gastrodiae Elata Pharmacopuncure at GB20 on motor control and cognitive dysfunction recovery after mild traumatic brain injury in rats. Rats were divided into three groups; (1) no treatment after traumatic brain injury(experiment I), (2) Treatment with NPA after traumatic brain injury(experiment II), (3) Treatment with GEP after traumatic brain injury(experiment III). In our study, we carried out behavioral test(Rotarod, Morris water maze) and immunohistochemistry study of the change BDNF in the hippocampus(pre, $7^{th}$, $14^{th}$ day). In Rotarod test(motor control function) was significantly increased in the experimental group III as compared with experimental group I, II on $7^{th}$(p<0.01) and $14^{th}$ day(p<0.001). In Morris water maze test(cognitive function) was significantly decreased in the experimental group III as compared with experimental group I, II on $14^{th}$ day(p<0.001). In immunohistochemistric response of BDNF in the hippocampus, the experimental group III was more immune response than the other groups on $14^{th}$ day. These results imply that Gastrodiae Elata Pharmacopuncure at GB20 can play a role in facilitating recovery of motor control and cognitive function after mild traumatic brain injury in rats.

• Nutrition Research and Practice
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• 제15권2호
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• pp.173-186
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• 2021

BACKGROUD/OBJECTIVES: Alzheimer's disease (AD) is the most common cause of dementia in the elderly. Due to the increased incidence of dementia, there is a corresponding increase concerning the importance of AD. In this study, we investigated the protective effects conferred by Zizyphus jujuba (Zj) and Zizyphus jujuba fermented by yeast (Zj-Y), on cognitive impairment in an AD mouse model. MATERIALS/METHODS: AD was induced by injecting amyloid beta25-35 (Aβ25-35) in ICR mice, and subsequently 200 mg/kg Zj or Zj-Y was administered daily for 14 days. The cognitive ability of AD mice was observed through behavioral experiments in T-maze, novel object recognition, and Morris water maze tests. We subsequently measured the levels of malondialdehyde (MDA), nitric oxide (NO), aspartate aminotransferase, and alanine aminotransferase in either tissues or serum. RESULTS: In behavioral tests, deterioration was revealed in the short- and long-term learning and memory functions in the Aβ25-35-injected control group compared to the normal group, indicating that Aβ25-35 injection impairs cognitive functions. However, administration of Zj and Zj-Y improved cognitive function in mice, as compared to the Aβ25-35-injected control mice. In addition, the Aβ25-35 induced elevations of MDA and NO in the brain, kidney, and liver were suppressed after exposure to Zj and Zj-Y. Especially, Zj-Y showed stronger scavenging effect against MDA and NO, as compared to Zj. CONCLUSIONS: Results of the present study indicate that Zj-Y exerts a protective effect on cognitive impairment and memory dysfunction, which is exerted by attenuating the oxidative stress induced by Aβ25-35.

• Journal of Ginseng Research
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• 제47권6호
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• pp.735-742
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• 2023

Background: Gintonin is a new material of ginseng that acts through the ginseng-derived lysophosphatidic acid (LPA) receptor ligand. The gintonin-enriched fraction (GEF) inhibits amyloid plaque accumulation in the cortex and hippocampus, improves cognitive dysfunction by increasing acetylcholine levels, and promoted hippocampal neurogenesis in an animal model of Alzheimer's disease. We evaluated the effect of the GEF on the cognitive performance of subjects with subjective memory impairment (SMI). Methods: In this eight-week, randomized, assessor- and participant-blinded, placebo-controlled study, participants with SMI were assigned to three groups receiving placebo, GEF 300 mg/day or GEF 600 mg/day. The Korean versions of the Alzheimer's Disease Assessment Scale (K-ADAS), Mini-Mental State Examination (K-MMSE), and Stroop color-word test (K-SCWT) were also evaluated along with the safety profiles. Results: One hundred thirty-six participants completed the study. After eight weeks, we analyzed intergroup differences in primary or secondary outcome score changes. When we compared the GEF group with the placebo group, we observed significant improvements in the K-ADAS and K-SCWT scores. The GEF group did not show a significant improvement in K-MMSE and BDI scores compared to the placebo group. No adverse events were observed in the gintonin and placebo groups for eight weeks. Conclusion: The GEF is safe and effective in improving subjective cognitive impairment related to both the K-ADAS and K-SCWT in this study. However, further large-scale and randomized controlled studies are warranted to secure other cognitive function tests besides the K-ADAS and K-SCWT, and to confirm the findings of the current study.