• Korean Journal of Medicinal Crop Science
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• v.25 no.6
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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.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.3
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• pp.201-209
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• 2014

The present study was designed to investigate the efficacy of selective $ET_A$ receptor antagonist, ambrisentan on hyperhomocysteinemia-induced experimental vascular dementia. L-methionine was administered for 8 weeks to induce hyperhomocysteinemia and associated vascular dementia in male rats. Ambrisentan was administered to L-methionine-treated effect rats for 4 weeks (starting from $5^{th}$ to $8^{th}$ week of L-methionine treatment). On $52^{nd}$ day onward, the animals were exposed to the Morris water maze (MWM) for testing their learning and memory abilities. Vascular endothelial function, serum nitrite/nitrate levels, brain thiobarbituric acid reactive species (TBARS), brain reduced glutathione (GSH) levels, and brain acetylcholinesterase (AChE) activity were also measured. L-methionine-treated animals showed significant learning and memory impairment, endothelial dysfunction, decrease in/serum nitrite/nitrate and brain GSH levels along with an increase in brain TBARS levels and AChE activity. Ambrisentan significantly improved hyperhomocysteinemia-induced impairment of learning, memory, endothelial dysfunction, and changes in various biochemical parameters. These effects were comparable to that of donepezil serving as positive control. It is concluded that ambrisentan, a selective $ET_A$ receptor antagonist may be considered as a potential pharmacological agent for the management of hyperhomocysteinemia-induced vascular dementia.

• Biomolecules & Therapeutics
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• v.22 no.3
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• pp.232-238
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• 2014

Alzheimer's disease (AD) is the most common neurodegenerative disease without known ways to cure. A key neuropathologic manifestation of the disease is extracellular deposition of beta-amyloid peptide (Ab). Specific mechanisms underlying the development of the disease have not yet been fully understood. In this study, we investigated effects of 4-O-methylhonokiol on memory dysfunction in APP/PS1 double transgenic mice. 4-O-methylhonokiol (1 mg/kg for 3 month) significantly reduced deficit in learning and memory of the transgenic mice, as determined by the Morris water maze test and step-through passive avoidance test. Our biochemical analysis suggested that 4-O-methylhonokiol ameliorated $A{\beta}$ accumulation in the cortex and hippocampus via reduction in beta-site APP-cleaving enzyme 1 expression. In addition, 4-O-methylhonokiol attenuated lipid peroxidation and elevated glutathione peroxidase activity in the double transgenic mice brains. Thus, suppressive effects of 4-O-methylhonokiol on $A{\beta}$ generation and oxidative stress in the brains of transgenic mice may be responsible for the enhancement in cognitive function. These results suggest that the natural compound has potential to intervene memory deficit and progressive neurodegeneration in AD patients.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.131-139
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• 2001

This study was conducted to evaluate the effect of PTSD on memory function and hippocampal volume, and to identify major variables correlated to hippocampal volume and memory function. Thirty four Vietnam veterans were collected for this study, among whom eighteen were PTSD patients and sixteen were combat control subjects. The author used Impact of Event Scale(IES), Combat Exposure Scale(CES), Hamilton Depression Rating Scale(HDRS) and Beck Depression Inventory (BDI). Korea Memory Assessment Scale(K-MAS) was assessed for memory function. Magnetic resonance imaging(MRI) was used to measure hippocampal volume. There were significant differences between PTSD and Non-PTSD veterans in IES, HDRS and BDI. Significant difference was found in verbal memory and total memory of K-MAS between PTSD and Non-PTSD veterans. There was significant difference in hippocampal volume between PTSD and Non-PTSD veterans. Short term memory, verbal memory and total memory were positively correlated to hippocampal volume. Hippocampal volume was negatively correlated to IES, HDRS, and BDI. These results suggest that PTSD severity be associated with hippocampal atrophy and memory dysfunction. Reduced or smaller hippocampal volume may be preexisting risk factor for stress exposure or the development of PTSD on combat exposure.

• Korean Journal of Biological Psychiatry
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• v.18 no.3
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• pp.141-147
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• 2011

Objectives The purpose of this study is to evaluate the relationship between the severity of white matter changes (WMC), risk factors and cognitive domains, including executive function profiles. Method Forty nine subjects over 55 years with subjective memory complaints were assessed with MRI and neuropsychological tests. The WMC were assessed by MRI T2-FLAIR images and divided into 3 groups of mild vs. moderate vs. severe and 2 groups of mild-moderate vs. severe by using Mantyla's criteria and Fazeka's criteria. The risk factors were examined in hypertension, heart disease history and chemistry Lab. Medical conditions which affect to cognitive dysfunction and definite dementia were also excluded. Results Comparing 3 groups, hypertension was identified as a risk factor of the WMC. Comparing 2 groups, total cholesterol and LDL were identified for as the risk factor of WMC. The severity of WMC was significantly associated with cognitive disturbances and their main effect on cognition was working memory and inhibition. Conclusion The risk factors of the WMC in the elderly were hypertension, hyperlipidemia. The severity of WMC appears to be associated with executive dysfunction in the elderly.

• Korean Journal of Biological Psychiatry
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• v.15 no.1
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• pp.46-53
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• 2008

Posterior cortical atrophy(PCA) is a presenile dementia that presents primarily with signs and symptoms of cortical visual dysfunction, while memory is relatively preserved until the late stage of the disease. We report a patient with PCA, confirmed by brain magnetic resonance imaging (MRI) and $F^{18}$-fluorodeoxyglucose positron emission tomography(FDG PET). A 58-year-old right-handed woman presented initially with visual dimness and difficulty finding things around her. She had partial Balint's syndrome, partial Gerstmann syndrome, and idiomotor apraxia. She also had a mild memory disturbance, but preserved insight of her disease. Neuropsychological evaluation showed decreased parietal and left temporal functions bilaterally. Brain MRI and $F^{18}$-FDG PET revealed typical bilateral occipitoparietal atrophy and hypometabolism, which were slightly worse on the right side. Cholinesterase inhibitor administration for 6 months improved the memory impairment slightly, but not the cortical visual dysfunction. This is a typical case of PCA, confirmed by neurologic signs and imaging findings.

• Journal of Acupuncture Research
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• v.23 no.2
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• pp.33-46
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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 extracellular deposition of beta-amyloid peptide $(A{\beta})$ in cerebral plaques. $A{\beta}$ is derived from the ${\beta}-amyloid$ precursor protein (APP) by the enzymes, ${\beta}-$ and ${\eta}o-secretase$. Compounds that ${\beta}-$ or ${\eta}o-secretase$ inhibit activity, can reduce the production of $A{\beta}$ peptides, and thus have therapeutic potential in the treatment of AD. Increasing body of evidence has been demonstrated that Bee Venom(BV) Acupuncture 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 $NF-{\kappa}B$. In this study, I investigated possible effects of BV on memory dysfunction caused by lipopolysaccharide (LPS) and $A{\beta}$ through inhibition of secretases activities and $A{\beta}$ aggregation. I examined the improving effect of BV on the LPS (2.5 mg/Kg, i.p.)-induced memory dysfunction using passive avoidance response and water maze tests in the mice. BV (0.84, $1.67\;{\mu}g/ml$) reversed the LPS-induced memorial dysfunction in dose dependent manner. BV also dose-dependently attenuated LPS-induced ${\beta}$ and ${\eta}o-secretase$ 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.

• Journal of The Korean Society of Clinical Toxicology
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• v.14 no.2
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• pp.115-121
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• 2016

Purpose: Because carbon monoxide (CO)-intoxicated patients with an alert mental status and only mild cognitive dysfunction may be inadequately assessed by traditional bedside neurologic examination in the emergency department (ED), they may not receive appropriate treatment. Methods: We retrospectively investigated the incidence and features of cognitive dysfunction using the Korean version of the Mini-Mental State Examination (MMSE-K) in ED patients with CO poisoning with alert mental status. We conducted a retrospective review of 43 consecutive mild CO poisoned patients with a Glasgow Coma Scale score of 15 based on documentation by the treating emergency physician in the ED between July 2014 and August 2015. Results: Cognitive dysfunction, defined as a score of less than 24 in the MMSE-K, was diagnosed in six patients (14%) in the ED. In the MMSE-K, orientation to time, memory recall, and concentration/calculation showed greater impairments. The mean age was significantly older in the cognitive dysfunction group than the non-cognitive dysfunction group (45.3 yrs vs. 66.5 yrs, p<0.001). Among the initial symptoms, experience of a transient change in mental status before ED arrival was significantly more common in the cognitive dysfunction group (32.4% vs. 100%, p=0.003). Conclusion: Patients with CO poisoning and an alert mental status may experience cognitive dysfunction as assessed using the MMSE-K during the early stages of evaluation in the ED. In the MMSE-K, orientation to time, memory recall, and concentration/calculation showed the greatest impairment.

• BMB Reports
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• v.54 no.6
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• pp.295-304
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• 2021

Olfactory neuropathology is a cause of olfactory loss in Alzheimer's disease (AD). Olfactory dysfunction is also associated with memory and cognitive dysfunction and is an incidental finding of AD dementia. Here we review neuropathological research on the olfactory system in AD, considering both structural and functional evidence. Experimental and clinical findings identify olfactory dysfunction as an early indicator of AD. In keeping with this, amyloid-β production and neuroinflammation are related to underlying causes of impaired olfaction. Notably, physiological features of the spatial map in the olfactory system suggest the evidence of ongoing neurodegeneration. Our aim in this review is to examine olfactory pathology findings essential to identifying mechanisms of olfactory dysfunction in the development of AD in hopes of supporting investigations leading towards revealing potential diagnostic methods and causes of early pathogenesis in the olfactory system.

• Korean Journal of Biological Psychiatry
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• v.13 no.1
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• pp.38-42
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• 2006

The case of a 66- year-old woman with coexisting idiopathic basal ganglia calcification(IBGC) and dementia was presented. The calcification was detected in bilateral basal ganglia, dentate nucleus, and thalamus by brain imaging. Serum calcium and phosphorus levels were normal. The underlying diseases of calcification of basal ganglia such as parathyroid dysfunction and other infectious, toxic, or metabolic illness were excluded. The patient had memory impairment and frontal executive dysfunction without aphasia, agnosia, apraxia, and visuospatial impairment in neuropsychological test. It suggested that the cognitive impairment might be due to the dysfunction of frontal-subcortical circuit.