• 동의신경정신과학회지
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• 제22권2호
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• pp.107-128
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• 2011

Objectives : This experiment was designed to investigate the efficacy of DDTCMT hot water extract & ultra-fine powder on Alzheimer's Disease Model. Methods : The effects of the DDTCMT hot water extract on expression of IL-$1{\beta}$, IL-6, TNF-${\alpha}$, COX-2, NOS-II, IL-10, IL-1 receptor antagonist mRNA and production of IL-$1{\beta}$, IL-6, TNF-${\alpha}$ in BV2 microglial cell line treated by lipopolysacchaide(LPS) were investigated. Expression of NO, ROS in BV2 microglial cell line treated by LPS and AChE activity in PC-12 cell treated by NGF were investigated. anti-AChE was observed through Western blot analysis. The effects of the DDTCMT hot water extract & ultra-fine powder on the behavior of the memory deficit mice induced by scopolamine were investigated. Results : 1. The DDTCMT hot water extract significantly decreased the production of mIL-6, mNOS-II, mTNF-${\alpha}$, and increased the production of mIL-10, mIL-1 receptor antagonist. 2. The DDTCMT hot water extract significantly suppressed the production of IL-$1{\beta}$, IL-6, TNF-${\alpha}$ in BV2 microglial cell line treated by LPS. 3. The DDTCMT hot water extract significantly suppressed the NO and ROS production in BV2 microglial cell line treated by LPS. 4. The DDTCMT hot water extract groups showed inhibition of AChE activity in NGF treated PC-12 cell line. 5. The DDTCMT hot water extract suppressed anti-AChE expression in NGF treated PC-12 cell line was observed by Western blot analysis. 6. The DDTCMT hot water extract & ultra-fine powder groups showed significantly inhibitory effect on the scopolamine -induced impairment of memory in the experiment of Morris water maze. Conclusions : These results suggest that the DDTCMT hot water extract & ultra-fine powder may be effective for the prevention and treatment of Alzheimer's disease.

• 동의신경정신과학회지
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• 제21권2호
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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.

• 한국감성과학회:학술대회논문집
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• 한국감성과학회 2003년도 춘계학술대회 논문집
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• pp.94-100
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• 2003

Patients with schizophrenia have thinking disorders such as delusion or hallucination, because they have a deficit in the ability which to systematize and integrate information. Therefore, they cannot integrate or systemize visual, auditory and tactile stimuli. In this study we suggest a virtual reality system for the assessment of cognitive ability of schizophrenia patients, based on the brain multimodal integration model. The virtual reality system provides multimodal stimuli, such as visual and auditory stimuli, to the patient, and can evaluate the patient's multimodal integration and working memory integration abilities by making the patient interpret and react to multimodal stimuli, which must be remembered for a given period of time. The clinical study showed that the virtual reality program developed is comparable to those of the WCST and the SPM.

• Perspectives in Nursing Science
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• 제9권1호
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• pp.45-50
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• 2012

Purpose: Despite poor cognitive function in heart failure (HF), few studies have examined cognition and its probable implication in self-care among Korean HF patients. The purposes of this study were (1) to describe cognition in the domains of global, memory, and executive functions, (2) to explore the relationship between cognition and self-care, and (3) to determine the amount of dietary sodium intake among Korean HF patients. Methods: A pilot study was conducted: 7 HF patients (3 men, mean age 68 years) completed face-to-face interviews for neuropsychological tests of cognition and self-care including dietary sodium intake. Results: More than half of the patients had impaired global cognition, memory, or executive function; patients with more severe HF were at higher risk of poor cognitive function. Korean HF patients exhibited poor self-care, with a high dietary sodium intake (5.6 g/day), approximately twice more than the suggested guideline of 2~3 g/day for patients with stable HF. Conclusion: Cognitive dysfunction and inadequate self-care with noncompliance with dietary sodium restriction were evident in Korean HF patients. More studies are warranted that examine the prevalence of cognitive impairment and areas of deficit using neuropsychological tests in a larger sample and that examine how cognition affects self-care and compliance in salt-intake.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• 제24권4호
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• pp.220-227
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• 2013

Objectives : This study aims to investigate the clinical characteristics and neuropsychological profiles of children with attention-deficit hyperactivity disorder (ADHD) and their siblings. Methods : Eighteen children (age $8.2{\pm}1.7$ years, 12 boys) with ADHD and their 18 siblings (age $7.8{\pm}1.6$ years, 8 boys) completed Continuous Performance (CPT), Stroop, Children's Trail Making, Rey-Kim Memory, and Kim's Frontal Executive Function tasks. The parents of these subjects underwent the Attention-Deficit/Hyperactivity Disorder Rating Scale (ARS), 10-item Parent General Behavior Inventory (P-GBI), and the Social Responsiveness Scale (SRS). Paired t-tests were used. Results : The inattention (p=.020), and hyperactivity-impulsivity (p=.001), scores of the ARS and the P-GBI score (p=.004) were significantly higher in children with ADHD than in their siblings. Deficits in social communication and motivation on SRS were higher in children with ADHD than in their siblings (p=.017 and p=.011, respectively). Z-scores of omission and commission errors as well as response time variability on visual CPT and omission errors on auditory CPT were in clinically significant range, and z-score of omission errors on auditory CPT was in borderline range in siblings. Omission (p=.018) and commission errors on Visual CPT (p=.007) were significantly higher in children with ADHD compared to their siblings. Recognition efficiency on Kim's Frontal Executive Function Task was lower in children with ADHD compared to their siblings, but in normal range in both groups. Stroop interference and figure fluency on Kims Frontal Executive Function Task were in borderline range in ADHD group, and figure fluency was in borderline range in siblings. Conclusion : Our results support a preliminary evidence for mild degree of attention deficit in ADHD siblings. Further studies are needed to examine the cognitive functions of siblings with ADHD in larger samples.

• The Korean Journal of Physiology and Pharmacology
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• 제17권4호
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• pp.331-338
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• 2013

AMP-activated protein kinase (AMPK), an important regulator of energy metabolism, is activated in response to cellular stress when intracellular levels of AMP increase. We investigated the neuroprotective effects of AMPK against scopolamine-induced memory impairment in vivo and glutamate-induced cytotoxicity in vitro. An adenovirus expressing AMPK wild type alpha subunit (WT) or a dominant negative form (DN) was injected into the hippocampus of rats using a stereotaxic apparatus. The AMPK WT-injected rats showed significant reversal of the scopolamine induced cognitive deficit as evaluated by escape latency in the Morris water maze. In addition, they showed enhanced acetylcholinesterase (AChE)-reactive neurons in the hippocampus, implying increased cholinergic activity in response to AMPK. We also studied the cellular mechanism by which AMPK protects against glutamate-induced cell death in primary cultured rat hippocampal neurons. We further demonstrated that AMPK WT-infected cells increased cell viability and reduced Annexin V positive hippocampal neurons. Western blot analysis indicated that AMPK WT-infected cells reduced the expression of Bax and had no effects on Bcl-2, which resulted in a decreased Bax/Bcl-2 ratio. These data suggest that AMPK is a useful cognitive impairment treatment target, and that its beneficial effects are mediated via the protective capacity of hippocampal neurons.

• 대한임상독성학회지
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• 제2권2호
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• pp.137-140
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• 2004

Acute cyanide poisoning is usually the result of attempted suicide which is often lethal within minutes or leads to a very poor prognosis after delayed and inadequate treatment. It affects the cerebral structures with the highest oxygen requirement, such as the basal ganglia, the cerebral cortex. We experienced a-45-year-old man who ingested Potassium Cyanide. He was stuporous. In 25 minutes, respiratory arrest developed and cardiopulmonary resuscitation was done. After return of spontaneous circulation, he admitted to intensive care unit, and conservative treatment was started. The clinical status was improved by degrees, but he couldn't perform daily activity like before. Minimal limitation of movement and memory deficit were left. In magnetic resonance imaging, which taken at the 11th day after admission, there were both basal ganglia and folia of cerebellum abnormality.

• 생물정신의학
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• 제7권1호
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• pp.55-63
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• 2000

Avariety of symptoms can occur following traumatic brain injury(TBI) or other types of acquired brain injury. These symptoms can include problems with short-term memory, attention, planning, problem solving, impulsivity, disinhibition, poor motivation, and other behavioral and cognitive deficit. These symptoms may respond to certain drugs, such as dopaminergic agents. Amantadine may protect patients from secondary neuronal damage after brain injury as a effect of NMDA receptor antagonists and may improve functioning of brain-injured patients as a dopaminergic agonist. Clinically, based on current evidence, amantadine may provide a potentially effective, safe, and inexpensive option for treating the cognitive, mood, and behavioral disorders of individuals with brain injury. The rationales for using amantadine are discussed, and pertinent literatures are reviewed.

• Natural Product Sciences
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• 제16권1호
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• pp.50-53
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• 2010

Cognitive enhancing activity of Betula plantyphylla sap was determined in scopolamine induced amnesic mice using passive avoidance test. Oral acute administration of the sap effectively reversed memory deficit in a dose dependent manner. Then the sap was standardized on the basis of sugar contents using HPLC combined with refractive index detector. Glucose and fructose were the main sugars present in the sap.

• Biomolecules & Therapeutics
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• 제28권5호
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• pp.381-388
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• 2020

Methamphetamine (METH) is a highly addictive psychostimulant and one of the most widely abused drugs worldwide. The continuous use of METH eventually leads to drug addiction and causes serious health complications, including attention deficit, memory loss and cognitive decline. These neurological complications are strongly associated with METH-induced neurotoxicity and neuroinflammation, which leads to neuronal cell death. The current review investigates the molecular mechanisms underlying METH-mediated neuronal damages. Our analysis demonstrates that the process of neuronal impairment by METH is closely related to oxidative stress, transcription factor activation, DNA damage, excitatory toxicity and various apoptosis pathways. Thus, we reach the conclusion here that METH-induced neuronal damages are attributed to the neurotoxic and neuroinflammatory effect of the drug. This review provides an insight into the mechanisms of METH addiction and contributes to the discovery of therapeutic targets on neurological impairment by METH abuse.