• Korean Journal of Biological Psychiatry
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• v.20 no.4
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• pp.119-128
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• 2013

Objectives Memory impairment is a very important mental health issue for elderly and adults. Mild cognitive impairment (MCI) is a prodromal stage of Alzheimer's disease (AD). Early detection of the prodromal stage of patients with AD is an important topic of interest for both mental health clinicians and policy makers. Methods Electroencephalograpgy (EEG) has been used as a possible biological marker for patients with MCI, and AD. In this review, we will summarize the clinical implications of EEG and ERP as a biological marker for AD and MCI. Results EEG power density, functional coupling, spectral coherence, synchronization, and connectivity were analyzed and proved their clinical efficacy in patients with the prodromal stage of AD. Serial studies on late event-related potentials (ERPs) were also conducted in MCI patients as well as healthy elders. Even though these EEG and ERP studies have some limitations for their design and method, their clinical implications are increasing rapidly. Conclusion EEG and ERP can be used as biological markers of AD and MCI. Also they can be used as useful tools for early detection of AD and MCI patients. They are useful and sensitive research tools for AD and MCI patients. However, some problems remain to be solved until they can be practical measures in clinical setting.

• Journal of Korean Biological Nursing Science
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• v.22 no.3
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• pp.172-175
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• 2020

Purpose: The purpose of this paper is to provide nurses with a concise review on neurodegenrative dementias. This review includes pathophysiology, clinical course, and tips on management of dementias from Alzheimer's disease (AD), Parkinson disease (PD) and lewy body dementia (LBD). Considering increasing numbers of dementia cases among older adults, nurses who are cognizant about dementia care are instrumental in maximizing daily activities and quality of life of patients with cognitive impairment and dementia.

• Journal of Ginseng Research
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• v.46 no.3
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• pp.464-472
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• 2022

Background: Gut microbiota influence the central nervous system through gut-brain-axis. They also affect the neurological disorders. Gut microbiota differs in patients with Alzheimer's disease (AD), as a potential factor that leads to progression of AD. Oral intake of Korean Red Ginseng (KRG) improves the cognitive functions. Therefore, it can be proposed that KRG affect the microbiota on the gut-brain-axis to the brain. Methods: Tg2576 were used for the experimental model of AD. They were divided into four groups: wild type (n = 6), AD mice (n = 6), AD mice with 30 mg/kg/day (n = 6) or 100 mg/kg/day (n = 6) of KRG. Following two weeks, changes in gut microbiota were analyzed by Illumina HiSeq4000 platform 16S gene sequencing. Microglial activation were evaluated by quantitative Western blot analyses of Iba-1 protein. Claudin-5, occludin, laminin and CD13 assay were conducted for Blood-brain barrier (BBB) integrity. Amyloid beta (Aβ) accumulation demonstrated through Aβ 42/40 ratio was accessed by ELISA, and cognition were monitored by Novel object location test. Results: KRG improved the cognitive behavior of mice (30 mg/kg/day p < 0.05; 100 mg/kg/day p < 0.01), and decreased Aβ 42/40 ratio (p < 0.01) indicating reduced Aβ accumulation. Increased Iba-1 (p < 0.001) for reduced microglial activation, and upregulation of Claudin-5 (p < 0.05) for decreased BBB permeability were shown. In particular, diversity of gut microbiota was altered (30 mg/kg/day q-value<0.05), showing increased population of Lactobacillus species. (30 mg/kg/day 411%; 100 mg/kg/day 1040%). Conclusions: KRG administration showed the Lactobacillus dominance in the gut microbiota. Improvement of AD pathology by KRG can be medicated through gut-brain axis in mice model of AD.

• Journal of Preventive Medicine and Public Health
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• v.49 no.2
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• pp.134-138
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• 2016

Objectives: Season of birth, an exogenous indicator of early life environment, has been related to higher risk of adverse psychiatric outcomes but the findings for Alzheimer's disease (AD) have been inconsistent. We investigated whether the month or season of birth are associated with AD. Methods: A nationwide nested case-control study including all community-dwellers with clinically verified AD diagnosed in 2005 to 2012 (n=70 719) and up to four age- sex- and region of residence-matched controls (n=282 862) residing in Finland. Associations between month and season of birth and AD were studied with conditional logistic regression. Results: Month of birth was not associated with AD (p=0.09). No strong associations were observed with season (p=0.13), although in comparison to winter births (December-February) summer births (June-August) were associated with higher odds of AD (odds ratio, 1.03; 95% confidence interval, 1.00 to 1.05). However, the absolute difference in prevalence in winter births was only 0.5% (prevalence of those born in winter were 31.7% and 32.2% for cases and controls, respectively). Conclusions: Although our findings do not support the hypothesis that season of birth is related to AD/dementia risk, they do not invalidate the developmental origins of health and disease hypothesis in late-life cognition. It is possible that season does not adequately capture the early life circumstances, or that other (postnatal) risk factors such as lifestyle or socioeconomic factors overrule the impact of prenatal and perinatal factors.

• Development and Reproduction
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• v.21 no.4
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• pp.417-424
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• 2017

Alzheimer's disease (AD) is neurodegenerative disease, characterized by the progressive decline of memory, cognitive functions, and changes in personality. The major pathological features in postmortem brains are neurofibrillary tangles and amyloid beta ($A{\beta}$) deposits. The majority of AD cases are sporadic and age-related. Although AD pathogenesis has not been established, aging and declining mitochondrial function has been associated. Mitochondrial dysfunction has been observed in AD patients' brains and AD mice models, and the mice with a genetic defect in mitochondrial complex I showed enhanced $A{\beta}$ level in vivo. To elucidate the role of mitochondrial complex I in AD, we used SH-SY5Y cells transfected with DNA constructs expressing human amyloid precursor protein (APP) or human Swedish APP mutant (APP-swe). The expression of APP-swe increased the level of $A{\beta}$ protein in comparison with control. When complex I was inhibited by rotenone, the increase of ROS level was remarkably higher in the cells overexpressing APP-swe compared to control. The number of dead cell was significantly increased in APP-swe-expressing cells by complex I inhibition. We suggest that complex I dysfunction accelerate amyloid toxicity and mitochondrial complex I dysfunction in aging may contribute to the pathogenesis of sporadic AD.

• Journal of Oriental Neuropsychiatry
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• v.21 no.2
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• pp.171-189
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• 2010

Objectives : This research investigates the effect of the HBSBS on Alzheimer's disease. Specifically, the effects of the HBSBS extract on (1) the behavior (2) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's disease mice induced with $\beta$A were investigated. Methods : The effects of the HBSBS extract suppressed the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and NOS-II mRNA in BV2 microglial cell line treated with LPS plus $\beta$A were investigated. The effects of the HBSBS extract on the behavior of the memory deficit mice induced by scopolamine were investigated. Results : 1. The HBSBS extract suppressed the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and NOS-II mRNA in BV2 microglial cell line treated with LPS plus $\beta$A. 2. The HBSBS extract suppressed the expression of $\beta$A protein production in BV2 microglial cell line treated with LPS plus $\beta$A. 3. The HBSBS extract showed significantly inhibitory effect on the scopolamine-induced impairment of memory in the experiment of Morris water maze. 4. The HBSBS group suppressed the over-expression of IL-1$\beta$ protein, TNF-$\alpha$ protein significantly in the mice with Alzheimer's disease induced by $\beta$A. 5. The HBSBS group reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by $\beta$A. 6. The HBSBS group reduced tau protein, and GFAP in the brain tissue of the mice with AD induced by $\beta$A. Conclusions : These results suggest that the HBSBS group may be effective for the treatment of AD. Thus, HBSBS could be considered among the future therapeutic drugs indicated for the treatment of AD.

• Journal of the Korean Chemical Society
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• v.60 no.2
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• pp.125-130
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• 2016

With the goal of developing Alzheimer’s disease therapeutics, we have designed and synthesized new triazole linked decursinol derivatives having potency inhibitory activities against cholinesterase [acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE)]. Since inhibition of cholinesterase (ChE) is still considered to be one of the most effective targets to treat AD patients, many new classes of ChE inhibitors have been synthesized. In an effort of identifying new type of cholinergic drug, decursinol derivatives 11-17 have been synthesized between decursinol and other biological interesting compounds such as lipoic acid, polyphenols, etc by using the click reaction and then evaluated their biological activities. Compound 12 (IC₅₀ = 5.89 ± 0.31 mM against BuChE) showed more effective inhibitory activity against BuChE than galantamine (IC₅₀ = 9.4 ± 2.5 mM). Decursinol derivatives can be considered a new class inhibitor for BuChE and can be applied to be a novel drug candidate to treat AD patients.

• Dementia and Neurocognitive Disorders
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• v.17 no.3
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• pp.90-99
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• 2018

Background and Purpose: To explore anatomic substrate of specific wandering patterns in patients with Alzheimer's disease (AD) by performing positron emission tomography with $^{18}F$ fluorodeoxyglucose positron emission tomography (FDG PET). Methods: Drug-naïve AD patients with wandering (n=80) and without wandering (n=262) were recruited. First, the specific pattern of wandering type was operationally classified according to specific wandering score and clinical assessment. Second, brain FDG PET was performed and fluorodeoxyglucose (FDG) uptake differences of specific brain regions according to wandering patterns were compared to those of non-wanderers. Results: In patients with pacing pattern, FDG PET showed significant lower FDG uptake in both middle cingulum and left putamen cluster compared to non-wanderers. The right precuneus and supplementary motor area in patients with random pattern and left calcarine sulcus, right calcarine sulcus, right middle cingulum, and right post central gyrus in patients with lapping pattern had significantly lower FDG uptake compared to non-wanderers. Conclusions: This study showed that wandering in patients with AD had three distinct patterns. These specific patterns showed significant lower FDG uptake in specific brain areas compared to non-wanderers.

• Journal of Dairy Science and Biotechnology
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• v.39 no.3
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• pp.94-103
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• 2021

The lack of an effective treatment for Alzheimer's disease (AD) stems primarily from incomplete understanding of AD's causes. A rapidly growing number of scientific reports highlight important roles played by peripheral infections and intestinal bacterial flora in pathological and physiological functions involving the microbiome-intestine-brain axis. The microbiome controls basic aspects of the central nervous system (CNS), immunity, and behavior, in health and disease. Changes in the density and composition of the microbiome have been linked to disorders of the immune, endocrine, and nervous systems, including mood changes, depression, increased susceptibility to stressors, and autistic behaviors. There is no doubt that in patients with AD, restoration of the intestinal microbiome to a composition reminiscent of that found in healthy adult humans will significantly slow the progression of neurodegeneration, by ameliorating inflammatory reactions and/or amyloidogenesis. In the near future, better understanding of bidirectional communication between the brain and microbiota will allow the development of functional diets using specific probiotic bacteria.

• Journal of the Korean Society of Radiology
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• v.81 no.3
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• pp.488-500
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• 2020

Accumulating evidence suggests that Alzheimer's disease (AD) is not only caused by accumulation of abnormal proteins, including amyloid and tau, but is also closely associated with abnormalities in the microvascular environment including the blood-brain barrier (BBB), both of which lead to neuroinflammation and neurodegeneration. Application of in vivo magnetic resonance imaging (MRI) has recently increased to assess BBB permeability in AD and related diseases. Here, we provide a narrative review of BBB permeability-related pathology in Alzheimer dementia and recent MRI research on BBB permeability changes in AD and related diseases. Furthermore, we briefly introduce the measurement of BBB permeability using MRI and its methodological issues.