• Clinical Psychopharmacology and Neuroscience
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• 제16권4호
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• pp.494-496
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• 2018

No previous reports have described a case in which deep brain stimulation elicited an acute mood swing from a depressive to manic state simply by switching one side of the bilateral deep brain stimulation electrode on and off. The patient was a 68-year-old woman with a 10-year history of Parkinson's disease. She underwent bilateral subthalamic deep brain stimulation surgery. After undergoing surgery, the patient exhibited hyperthymia. She was scheduled for admission. On the first day of admission, it was clear that resting tremors in the right limbs had relapsed and her hyperthymia had reverted to depression. It was discovered that the left-side electrode of the deep brain stimulation device was found to be accidentally turned off. As soon as the electrode was turned on, motor impairment improved and her mood switched from depression to mania. The authors speculate that the lateral balance of stimulation plays an important role in mood regulation. The current report provides an intriguing insight into possible mechanisms of mood swing in mood disorders.

• 농업과학연구
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• 제48권1호
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• pp.119-131
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• 2021

Over-produced reactive oxygen species (ROS) exert oxidative damage on lipids, proteins, and DNA in the human body, which leads to the onset of neurodegenerative diseases such as Alzheimer's disease (AD). In this study, we explored the cellular antioxidant effect of Cirsium japonicum var. maackii (CJM) against hydrogen peroxide (H₂O₂)-induced oxidative stress in neuronal cells. The antioxidant activity was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, 2',7'-dichlorofluorescin diacetate and nitric oxide (NO) assays, and the molecular mechanisms were examined by Western blot analysis. H₂O₂ treatment of SH-SY5Y cells decreased cell viability and increased ROS and NO production compared to H₂O₂-untreated cells. However, CJM increased cell viability and decreased ROS and NO accumulation in the H₂O₂-treated SH-SY5Y cells compared to H₂O₂-treated control cells. Especially, the EtOAc fraction from CJM showed the strongest antioxidant effect compared with the other extracts and fractions. Therefore, we further examined the CJM mechanism against oxidative stress using the EtOAc fraction from CJM. The EtOAc fraction up-regulated the expressions of heme oxygenase-1, NAD(P)H quinone oxidoreductase 1, and thioredoxin reductase 1. These results indicate that CJM promotes the activation of antioxidative enzymes, which eliminate ROS and NO, and further leads to an increase in the cell viability. Taken together, our results show that CJM exhibited an antioxidant activity in H₂O₂-treated SH-SY5Y cells, and it could be a novel antioxidant agent for the prevention or treatment of neurodegenerative disease such as AD.

• Nutrition Research and Practice
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• 제16권2호
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• pp.173-193
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• 2022

BACKGROUND/OBJECTIVES: Alzheimer's disease (AD) is one of the most representative neurodegenerative disease mainly caused by the excessive production of amyloid beta (Aβ). Several studies on the antioxidant activity and protective effects of Populus tomentiglandulosa (PT) against cerebral ischemia-induced neuronal damage have been reported. Based on this background, the present study investigated the protective effects of PT against cognitive impairment in AD. MATERIALS/METHODS: We orally administered PT (50 and 100 mg/kg/day) for 14 days in an Aβ_25-35-induced mouse model and conducted behavioral experiments to test cognitive ability. In addition, we evaluated the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum and measured the production of lipid peroxide, nitric oxide (NO), and reactive oxygen species (ROS) in tissues. RESULTS: PT treatment improved the space perceptive ability in the T-maze test, object cognitive ability in the novel object recognition test, and spatial learning/long-term memory in the Morris water-maze test. Moreover, the levels of AST and ALT were not significantly different among the groups, indicating that PT did not show liver toxicity. Furthermore, administration of PT significantly inhibited the production of lipid peroxide, NO, and ROS in the brain, liver, and kidney, suggesting that PT protected against oxidative stress. CONCLUSIONS: Our study demonstrated that administration of PT improved Aβ_25-35-induced cognitive impairment by regulating oxidative stress. Therefore, we propose that PT could be used as a natural agent for AD improvement.

• Molecules and Cells
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• 제47권1호
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• pp.100005.1-100005.15
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• 2024

Amyotrophic lateral sclerosis is a devastating neurodegenerative disease with a complex genetic basis, presenting both in familial and sporadic forms. The hexanucleotide (G₄C₂) repeat expansion in the C9orf72 gene, which triggers distinct pathogenic mechanisms, has been identified as a major contributor to familial and sporadic Amyotrophic lateral sclerosis cases. Animal models have proven pivotal in understanding these mechanisms; however, discrepancies between models due to variable transgene sequence, expression levels, and toxicity profiles complicate the translation of findings. Herein, we provide a systematic comparison of 7 publicly available Drosophila transgenes modeling the G₄C₂ expansion under uniform conditions, evaluating variations in their toxicity profiles. Further, we tested 3 previously characterized disease-modifying drugs in selected lines to uncover discrepancies among the tested strains. Our study not only deepens our understanding of the C9orf72 G₄C₂ mutations but also presents a framework for comparing constructs with minute structural differences. This work may be used to inform experimental designs to better model disease mechanisms and help guide the development of targeted interventions for neurodegenerative diseases, thus bridging the gap between model-based research and therapeutic application.

• Journal of Acupuncture Research
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• 제23권3호
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• pp.117-127
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• 2006

Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disease associated with aging in the human population. This disease is characterized by the following 4 structural changes : Atrophy of the Cortex, Parasympathetic, and other neural cells, the existence of Neurofibrillary tangles (NFTs), and the accumulation of Senile plaques. NFTs and Senile plaques is known to be the index of this disease. Senile plaques disturbs the neutro transmission and depletes of Acetylcholine. So, Recovery of Acetylcholine is the primal objective for treating Alzheimer's disease. So, Inhibiting the activity of Acetylcholine Esterase (AChE), which causes the hydrolysus of acetylcholine into choline and acetate, can be seen as a key role for treating Alzheimer's disease. Increasing body of evidence has been demonstrated that Bee Venom Acupuncture (BV) could compete with complex protein involving in multiple step of $NF-_{\kappa}B$ activation and exert the anti-inflammatory potential of combined inhibition of the prostanoid and nitric oxide synthesis systems by inhibition of IKK and $NF-_{\kappa}B$. BV dose-dependently attenuated Scopolamine-induced Acetylcholine esterase activities in cerebral cortex and hippocampus of the mice brain. This study therefore suggests that BV acupuncture method may be useful for prevention of development or progression of AD.

• BMB Reports
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• 제52권4호
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• pp.250-258
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• 2019

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by selective and progressive loss of dopaminergic neurons. Genetic and environmental risk factors are associated with this disease. The genetic factors are composed of approximately 20 genes, such as SNCA, parkin, PTEN-induced kinase1 (pink1), leucine-rich repeat kinase 2 (LRRK2), ATP13A2, MAPT, VPS35, and DJ-1, whereas the environmental factors consist of oxidative stress-induced toxins such as 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), rotenone, and paraquat. The analyses of their functions and mechanisms have provided important insights into the disease process, which has demonstrated that these factors cause oxidative damage and mitochondrial dysfunction. The most invaluable studies have been performed using disease model organisms, such as mice, fruit flies, and worms. Among them, Drosophila melanogaster has emerged as an excellent model organism to study both environmental and genetic factors and provide insights to the pathways relevant for PD pathogenesis, facilitating development of therapeutic strategies. In this review, we have focused on the fly model organism to summarize recent progress, including pathogenesis, neuroprotective compounds, and newer approaches.

• BMB Reports
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• 제43권10호
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• pp.649-655
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• 2010

Alzheimer's disease (AD) is the most common age-dependent neurodegenerative disorder and shows progressive memory loss and cognitive decline. Intraneuronal filaments composed of aggregated hyperphosphorylated tau protein, called neurofibrillary tangles, along with extracellular accumulations of amyloid $\beta$ protein (A$\beta$), called senile plaques, are known to be the neuropathological hallmarks of AD. In light of recent studies, epigenetic modification has emerged as one of the pathogenic mechanisms of AD. Epigenetic changes encompass an array of molecular modifications to both DNA and chromatin, including transcription factors and cofactors. In this review, we summarize how DNA methylation and changes to DNA chromatin packaging by post-translational histone modification are involved in AD. In addition, we describe the role of SIRTs, histone deacetylases, and the effect of SIRT-modulating drugs on AD. Lastly, we discuss how amyloid precursor protein (APP) intracellular domain (AICD) regulates neuronal transcription. Our understanding of the epigenomes and transcriptomes of AD may warrant future identification of novel biological markers and beneficial therapeutic targets for AD.

• Natural Product Sciences
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• 제15권3호
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• pp.125-129
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• 2009

Neurodegenerative diseases such as Alzheimer's disease, stroke, and Parkinson's disease, are caused by neuronal cell death. Apoptosis, oxidative stress, inflammation, excitotoxicity or ischemia are discussed to play a role of neuronal cell death. In order to find the candidate of neuroprotective agent, neuroprotective activity of some medicinal plants was investigated with in vitro assay system using glutamate-induced neurotoxicity in primary cultures of rat cortical cells. The aqueous methanolic extracts of twenty-seven medicinal plants were evaluated the protective effects against glutamate-injured excitotoxicity in rat cortical cells at the concentration of 50 $\mu$g/ml and 100 $\mu$g/ml, respectively. Among them, extracts of Lonicera japonica, Taraxacum platycarpum, Polygonum aviculare, Gardenia jasminoides, Forsythia viridissima, Lygodium japonicum, Panax notoginseng, Akebia quinata, Anemarrhena asphodeloides and Phellodendron amurense showed significantly neuroprotective activities against glutamate-induced neurotoxicity in primary rat cortical cells.

• Journal of Microbiology and Biotechnology
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• 제26권9호
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• pp.1657-1660
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• 2016

Prion diseases are incurable neurodegenerative disorders. Our previous study demonstrated that polylysine was effective in prolonging the incubation period in a rodent model and in alleviating the scrapie prion protein (PrP^Sc) burden in the brain at the terminal stage of the disease. Here, we report that intraperitoneal administration of polylysine suppresses the accumulation of prions in the spleen during the early stages of the disease. This study supports the congruence of PrP^Sc inhibition by polylysine in both the spleen and brain.

• 한국자기공명학회논문지
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• 제24권2호
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• pp.43-46
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• 2020

Huntington's disease (HD) is an inherited neurodegenerative disease caused by abnormal polyglutamine (polyQ) expansion in the huntingtin protein (Htt). There is no cure for HD so far. Although exact molecular mechanism of HD pathogenesis is still elusive, fibril formation of the expanded Htt is linked to the toxicity. In this study, we prepared the expanded Htt containing 46 glutamines, and induced the fibrillation by proteolytic cleavage. Fibrillation of the pathogenic Htt has been monitored by time course NMR experiment. The NMR-based monitoring method could be widely used to screen the candidates to inhibit the fibrillation of the pathogenic Htt.