• Molecules and Cells
• /
• v.40 no.9
• /
• pp.613-620
• /
• 2017

The most common form of senile dementia is Alzheimer's disease (AD), which is characterized by the extracellular deposition of amyloid ${\beta}-peptide$ ($A{\beta}$) plaques and the intracellular formation of neurofibrillary tangles (NFTs) in the cerebral cortex. Tau abnormalities are commonly observed in many neurodegenerative diseases including AD, Parkinson's disease, and Pick's disease. Interestingly, tau-mediated formation of NFTs in AD brains shows better correlation with cognitive impairment than $A{\beta}$ plaque accumulation; pathological tau alone is sufficient to elicit frontotemporal dementia, but it does not cause AD. A growing amount of evidence suggests that soluble $A{\beta}$ oligomers in concert with hyperphosphorylated tau (pTau) serve as the major pathogenic drivers of neurodegeneration in AD. Increased $A{\beta}$ oligomers trigger neuronal dysfunction and network alternations in learning and memory circuitry prior to clinical onset of AD, leading to cognitive decline. Furthermore, accumulated damage to mitochondria in the course of aging, which is the best-known nongenetic risk factor for AD, may collaborate with soluble $A{\beta}$ and pTau to induce synapse loss and cognitive impairment in AD. In this review, I summarize and discuss the current knowledge of the molecular and cellular biology of AD and also the mechanisms that underlie $A{\beta}-mediated$ neurodegeneration.

• Journal of Preventive Medicine and Public Health
• /
• v.51 no.1
• /
• pp.1-5
• /
• 2018

Smokers keep smoking despite knowing that tobacco claims many lives, including their own and others'. What makes it hard for them to quit smoking nonetheless? Tobacco companies insist that smokers choose to smoke, according to their right to self-determination. Moreover, they insist that with motivation and willpower to quit smoking, smokers can easily stop smoking. Against this backdrop, this paper aims to discuss the addictive disease called tobacco use disorder, with an assessment of the addictiveness of tobacco and the reasons why smoking cessation is challenging, based on neuroscientific research. Nicotine that enters the body via smoking is rapidly transmitted to the central nervous system and causes various effects, including an arousal response. The changes in the nicotine receptors in the brain due to continuous smoking lead to addiction symptoms such as tolerance, craving, and withdrawal. Compared with other addictive substances, including alcohol and opioids, tobacco is more likely to cause dependence in smokers, and smokers are less likely to recover from their dependence. Moreover, the thinning of the cerebral cortex and the decrease in cognitive functions that occur with aging accelerate with smoking. Such changes occur in the structure and functions of the brain in proportion to the amount and period of smoking. In particular, abnormalities in the neural circuits that control cognition and decision-making cause loss of the ability to exert self-control and autonomy. This initiates nicotine dependence and the continuation of addictive behaviors. Therefore, smoking is considered to be a behavior that is repeated due to dependence on an addictive substance, nicotine, instead of one's choice by free will.

• Investigative Magnetic Resonance Imaging
• /
• v.7 no.1
• /
• pp.56-60
• /
• 2003

We present MR diffusion-weighted imaging (DWI) findings of status epilepticus in two patients. DWI showed a focal or diffuse hyperintensity with decreased apparent diffusion coefficient (ADC) value, indicating cytotoxic edema in th e cerebral hemispheric cortices. The hyperintensities were located in the bilateral temporoparietooccipital areas and insular cortex in one patient, and unilaterally in the temporal lobe in the other patient.

• Journal of Ginseng Research
• /
• v.35 no.4
• /
• pp.421-428
• /
• 2011

This study evaluated cholineresterase inhibitory activity of Korean white ginseng extract (WGE), red ginseng extract (RGE), and black ginseng extract (BGE) and the cholinergic effect on scopolamine (SCOP)-induced amnesic mice. WGE, RGE, and BGE inhibited acetylcholineserase (AChE), as well as butyrylcholineserase (BuChE) in a concentration-dependent manner. BGE presented strong inhibition of AChE with an $IC_{50}$ value of 1.72 mg/mL, followed by WGE (5.89 mg/mL), RGE (6.30 mg/mL), respectively. The inhibitory activity of the three ginseng extracts on BuChE showed similar values among the groups. To better understand the mechanisms of the possible effect of ginseng extract on the cholinergic function, this study assessed the expression of the cholinergic markers of choline acetyltransferase (ChAT) and AChE using western blot and RT-PCR analysis in the brains of amnesic mice. Treatment with ginseng extracts led to inhibition of AChE expression and, the activation of ChAT expression in the hippocampus and the cerebral cortex of amnesic mice as induced by SCOP. The results suggest that ginseng extracts including BGE, appear to modulate the metabolism of acetylchoine (ACh), which would greatly increase synaptic ACh levels and most potently revert SCOP-induced amnesia.

• Toxicological Research
• /
• v.23 no.4
• /
• pp.311-319
• /
• 2007

Elevated blood levels of homocysteine (a sulfur-containing amino acid) have been linked to increased risk of cerebrovascular disease including Alzheimer's disease. A recent study suggests that elevated homocysteine levels may lead to replicative senescence in vitro called 'permanent arrest of cell cycle' caused by oxidative stress. In this study, serum homocysteine level in rat was reduced by Lentinus edodes-powder diet, resulting in the reduced level of oxidative stress in rat brain. In addition, homocysteine-induced replicative senescence treated with or without Lentinus edodes-powder was analyzed by population doubling in vitro. The Lentinus edodes-powder induced a increased number of population doubling in primary neuron cell isolated from rat-cerebral cortex. This indicates that Lentinus edodes-powder would delay a homocysteine-induced aging of neuron cells in brain, showing a possible role in preventing cerebrovascular diseases including Alzheimer's disease.

• Journal of Korean Neurosurgical Society
• /
• v.57 no.3
• /
• pp.204-207
• /
• 2015

We are reporting an unusual case of dural arteriovenous fistula (AVF) of the superior sagittal sinus (SSS) after tamoxifen treatment for breast cancer. A 30-year-old female arrived at the emergency room with a sudden headache and left sided weakness and sensory loss. In her past medical history, she was diagnosed with breast cancer 1 year prior, and subsequently underwent a breast conserving mastectomy with whole breast radiation and adjuvant chemotherapy with tamoxifen. At the time of admission, computed tomography showed a small acute intracerebral hemorrhage at the right parietal cortex, and magnetic resonance imaging showed that a dural AVF at the SSS with a prominent and tortuous venous enhancement along the centrum semiovale was present. Cerebral angiography showed that the dural AVF at the mid-portion of the SSS with meningeal arterial feeding vessels entering the wall of the SSS, then draining through the dilated cortical veins. Our patient had no signs of active malignancy or any abnormalities in her coagulation profile, so it can be concluded that the tamoxifen was the likely cause of the SSS thrombosis and dural AVF. The dural AVF was treated by an endovascular coil embolization for the arterialized segment of the SSS. The patient dramatically recovered favorably from left side motor and sensory deficit. The best clinical approach is to screen potential patients of tamoxifen hormonal therapy and educate them on the sign and symptoms of life threatening thromboembolic events while taking tamoxifen.

• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.4
• /
• pp.367-376
• /
• 1997

The effect of an organic peroxide, t-butylhydroperoxide (t-BHP), on glutamate uptake was studied in synaptosomes prepared from cerebral cortex. t-BHP inhibited the $Na^+-dependent$ glutamate uptake with no change in the $Na^+-independent$ uptake. This effect of t-BHP was not altered by addition of $Ca^{2+}$ channel blockers (verapamil, diltiazem and nifedipine) or $PLA_2$ inhibitors (dibucaine, butacaine and quinacrine). However, the effect was prevented by iron chelators (deferoxamine and phenanthroline) and phenolic antioxidants (N,N'-diphenyl-phenylenediamine, butylated hydroxyanisole, and butylated hydroxytoluene). At low concentrations (＜1.0 mM), t-BHP inhibited glutamate uptake without altering lipid peroxidation. Moreover, a large increase in lipid peroxidation by $ascorbate/Fe^{2+}$ was not accompanied by an inhibition of glutamate uptake. The impairment of glutamate uptake by t-BHP was not intimately related to the change in $Na^+-K+-ATPase$ activity. These results suggest that inhibition of glutamate uptake by t-BHP is not totally mediated by peroxidation of membrane lipid, but is associated with direct interactions of glutamate transport proteins with t-BHP metabolites. The $Ca^{2+}$ influx through $Ca^{2+}$ channel or $PLA_2$ activation may not be involved in the t-BHP inhibition of glutamate transport.

• Journal of Biomedical Engineering Research
• /
• v.22 no.2
• /
• pp.145-150
• /
• 2001

대뇌 피질에 삽입하여 깊이에 따라 신경 신호를 기록하기 위한 탐침형 반도체 미세전극 어레이(depth-type silicon microelectrode array, 일명 SNU probe)를 제작하였다. 붕소를 확산시켜 생성된 고농도 p-type doping된 p＋ 영역을 습식식각 정지점으로 사용하는 기존의 방법과 달리 실리콘 웨이퍼의 앞면을 건식식각하여 원하는 탐침 두께만큼의 깊이로 트렌치(trench)를 형성한 후 뒷면을 습식식각하는 방법으로 탐침 형태의 미세 구조를 만들었다. 제작된 반도체 미세전극 어레이의 탐침 두께는 30 $\mu\textrm{m}$이며 실리콘 건식식각을 위한 마스크로 6 $\mu\textrm{m}$ 두께의 LTO(low temperature oxide)를 사용하였다. 탐침의 두께는 개발된 본 공정을 이용해서 5~90 $\mu\textrm{m}$ 범위까지 쉽게 조절할 수 있었다. 탐침의 두께를 보다 쉽게 조절할 수 있게 됨에 따라 여러 신경조직에 필요한 다양한 구조의 반도체 미세전극 어레이를 개발할 수 있게 되었다. 본 공정을 이용해서 개발된 4채널 SUN probe를 사용하여 흰쥐의 제1차 체감각 피질에서 4채널 신경 신호를 동시에 기록하였으며, 전기적 특성검사에서 기존의 탐침형 반도체 미세전극, 텅스텐 전극과 대등하거나 우수한 신호대 잡음비(signal to noise ratio, SNR)특성을 가짐을 확인하였다.

• Journal of Magnetics
• /
• v.18 no.2
• /
• pp.192-196
• /
• 2013

We have investigated the changes of electroencephalography (EEG) and electrocardiography (ECG) under pulsed magnetic field (PMF) and acupuncture stimulus on acupoint PC9. In order to compare quantitatively the effect of PMF and acupuncture stimulus, the difference of alpha activities are calculated from EEG spectra, and the spectrum curves of ECG were analyzed in the frequency domain of heart rate variability (HRV). The increase of alpha activities after both stimuli could be explained that the impulse of stimulus on PC9 might pass through sensory nerve following meridian and approach the cerebral cortex, causing the central nervous system (CNS) to be activated for pacifying emotion and calming the mind. The decrease in sympathovagal activity of HRV after both stimuli indicates that parasympathetic nerves were activated and the sympathetic nerves were in constrained condition. These findings suggest that PMF could be patient-friendly alternative non-invasive medical treatment for influencing human physiology, in comparison with acupuncture inserting the needle and inducing nervous and anxious state to subject.

• Korean Journal of Acupuncture
• /
• v.23 no.2
• /
• pp.105-111
• /
• 2006

Objectives: We investigated the effect of electroacupuncture on epileptic rat model and its underlying mechanisms on suppression of the epilepsy. Methods: It was used pentylenetetrazol $(35{\sim}40\;mg/kg.\;i.p)$ induced epileptic rat model and square wave electrical stimulations (5 mA, 5, 40 or 80 Hz frequency) was applied to acupoints on 'Dazhui' and 'Taichong' for 30min. Results: Electroacupuncture suppressed spikes and slow waves of EEG due to the epileptic condition. Out of electroacupuncture, a high frequency of 80Hz had a better effect for suppress epileptic EEG wave. Conclusions: Electroacupuncture can markedly reduce the excitability of cerebral cortex and strengthen the inhibitory process, checking epilepsy wave. Some intrathalamic nuclei have a promoting or inhibiting effect on epileptic EEG wave. This experimental study we are proposed to Electro-acupuncture can suppression epileptic rat model and it's scientific mechanisms.