• Speech Sciences
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• v.15 no.2
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• pp.111-118
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• 2008

We identified the characteristic impairmants of linguistic semantic memory in patients with prodromal Alzheimer's disease(AD) and mild AD. To elucidate the earliest changes of semantic language function in subjects with AD, performances on confrontation naming test and verbal fluency task were compared among patients with AD patients (n=20), mild AD patients (n=27) and healthy elderly controls (n=20). Tasks in this study included the confrontation naming test of Test of Lexical Processing in Aphasia(TLPA/Japanese) and one-minute verbal fluency task (semantic/ phonetic categories). The results were as follows: 1) Performances of the prodromal AD group showed the comparable to those of the control group on the confrontation naming test, 2) In the semantic/phonetic verbal fluency tasks, the performances of the control group were better than those of the prodromal AD and mild AD groups, but no significant differences were shown between the prodromal AD and the mild AD group.

• Smart Media Journal
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• v.13 no.6
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• pp.90-97
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• 2024

This paper focuses on detecting Alzheimer's Disease (AD). The most usual form of dementia is Alzheimer's disease, which causes permanent cause memory cell damage. Alzheimer's disease, a neurodegenerative disease, increases slowly over time. For this matter, early detection of Alzheimer's disease is important. The purpose of this work is using Magnetic Resonance Imaging (MRI) to diagnose AD. A Convolution Neural Network (CNN) model, Reset, and VGG the pre-trained learning models are used. Performing analysis and validation of layers affects the effectiveness of the model. T1-weighted MRI images are taken for preprocessing from ADNI. The Dataset images are taken from the Alzheimer's Disease Neuroimaging Initiative (ADNI). 3D MRI scans into 2D image slices shows the optimization method in the training process while achieving 96% and 94% accuracy in VGG 16 and ResNet 18 respectively. This study aims to classify AD from brain 3D MRI images and obtain better results.

• Molecules and Cells
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• v.40 no.9
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• pp.613-620
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• 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 the Korean Society of Radiology
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• v.83 no.3
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• pp.486-507
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• 2022

Cerebral small vessel disease (CSVD) includes vascular lesions detected on brain MRI, such as white matter hyperintensities, lacunar infarctions, microbleeds, or enlarged perivascular spaces. There is accumulating evidence that vascular changes may play an important role in development of Alzheimer's disease (AD), and CSVD lesions detected on brain MRI were reported to be associated with β-amyloid and tau proteins accumulation. As the vascular contribution has therapeutic potential, it is important to understand the association of CSVD with AD and AD biomarkers. This review begins with a brief introduction of AD and AD biomarkers, explains the association between AD and vascular changes, and then details the pathogenesis and MR imaging findings of CSVD. Afterwards, we discuss the association of CSVD with AD and AD biomarkers.

• Sleep Medicine and Psychophysiology
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• v.9 no.1
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• pp.9-13
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• 2002

Alzheimer's disease (AD) is one of the most common and devastating dementing disorders of old age. Most AD patients showed significant alternation of sleep structure as well as cognitive deficit. Typical findings of sleep architecture in AD patients include lower sleep efficiency, higher stage 1 percentage, and greater frequency of arousals. The slowing of EEG activity is also noted. Abnormalities in REM sleep are of particular interest in AD because the cholinergic system is related to both REM sleep and AD. Several parameters representing REM sleep structure such as REM latency, the amount of REM sleep, and REM density are change in patients with AD. Especially, measurements of EEG slowing during tonic REM sleep can be used as an EEG marker for early detection of possible AD. In addition, a structural defect in the suprachiasmatic nucleus is suggested to cause various chronobiological alternations in AD. Most of alternations related to sleep make sleep disturbances common and disruptive symptoms of AD. In this article, the author reviewed the alternation of sleep structure and circadian rhythm in AD patients.

• BMB Reports
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• v.42 no.8
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• pp.467-474
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• 2009

The modification of proteins by reversible phosphorylation is a key mechanism in the regulation of various physiological functions. Abnormal protein kinase or phosphatase activity can cause disease by altering the phosphorylation of critical proteins in normal cellular and disease processes. Alzheimer' disease (AD), typically occurring in the elderly, is an irreversible, progressive brain disorder characterized by memory loss and cognitive decline. Accumulating evidence suggests that protein kinase and phosphatase activity are altered in the brain tissue of AD patients. Tau is a highly recognized phosphoprotein that undergoes hyperphosphorylation to form neurofibrillary tangles, a neuropathlogical hallmark with amyloid plaques in AD brains. This study is a brief overview of the altered protein phosphorylation pathways found in AD. Understanding the molecular mechanisms by which the activities of protein kinases and phosphatases are altered as well as the phosphorylation events in AD can potentially reveal novel insights into the role aberrant phosphorylation plays in the pathogenesis of AD, providing support for protein phosphorylation as a potential treatment strategy for AD.

• The Journal of Internal Korean Medicine
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• v.19 no.1
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• pp.291-300
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• 1998

Dementia is the neurodegenerative process that affects cognition, behavior and function and one of the most prominent diseases of dementia is Alzheimer's disease(AD). AD is a dementing illness characterized clinically by the progressive and irreversible deafferentation of the limbic system, association neocortex and basal forebrain. A number of conditions are known to be predisposing risk factors for AD. In several of these, initiation of glial-mediated inflammatory pathways as a mechanism of AD is getting a lot of attention. On the other hand, a biochemical marker for monitoring the onset and progression of the disease would be a valuable tool for disease management. Also such a marker might be used as an end point in clinical intervention protocols. This biochemical marker will have the potential for identifying subjects afflicted with the disease and possibly for monitoring the onset and longitudinal progression of the disease. Here we have reviewed the latest papers of different approaches to AD. Of course, there is a section of PET which is very useful clinically nowadays.

• BMB Reports
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• v.53 no.1
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• pp.10-19
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• 2020

Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain. The AD pathophysiology entails chronic inflammation involving innate immune cells including microglia, astrocytes, and other peripheral blood cells. Inflammatory mediators such as cytokines and complements are also linked to AD pathogenesis. Despite increasing evidence supporting the association between abnormal inflammation and AD, no well-established inflammatory biomarkers are currently available for AD. Since many reports have shown that abnormal inflammation precedes the outbreak of the disease, non-invasive and readily available peripheral inflammatory biomarkers should be considered as possible biomarkers for early diagnosis of AD. In this minireview, we introduce the peripheral biomarker candidates related to abnormal inflammation in AD and discuss their possible molecular mechanisms. Furthermore, we also summarize the current state of inflammatory biomarker research in clinical practice and molecular diagnostics. We believe this review will provide new insights into biomarker candidates for the early diagnosis of AD with systemic relevance to inflammation during AD pathogenesis.

• Journal of Preventive Medicine and Public Health
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• v.39 no.3
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• pp.243-248
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• 2006

Objectives: The Quality of Life-Alzheimer's Disease (QOL-AD) scale is a reliable and valid tool for assessing the quality of life (QOL) in the elderly with dementia. This study aimed to develop the Korean version of Quality of Life-Alzheimer's Disease (KQOL-AD) scale for the demented elderly living in the community. Methods: KQOL-AD was administered to two groups: 24 demented elderly and 72 cognitively impaired elderly with no dementia (CIND) who were living in the community Each elderly person and their caregiver rated the elderly QOL. The Korean version of mini-mental state examination (MMSE-K), the clinical dementia rating (CDR), the activities of daily living (ADL), and the neuropsychiatric inventory (NPI) were also assessed. The reliability and validity of the KQOL-AD were examined. Results: In the dementia group, the internal consistency (Cronbach's $\alpha$), the split half and the test-retest reliabilities of the KQOL-AD were excellent. Scores on the KQOL-AD were significantly correlated with the scores of the NPI, but they were not significantly correlated with scores of the MMSE-K, CDR and ADL. In addition, the CIND group showed similar results to the dementia group. Conclusions: KQOL-AD might be a reliable and valid instrument for assessing QOL in the elderly with dementia It could be used as an important outcome measure for research on the demented elderly.

• Herbal Formula Science
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• v.11 no.2
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• pp.95-110
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• 2003

Alzheimer's disease(AD) is a geriatric dementia that is widespread in old age. In the near future AD will be the biggest problem in public health service. Although a variety of oriental prescriptions in study Jeonmaedan have been traditionally utilized for the treatment of AD, their pharmacological effects and action mechanisms have not yet fully elucidated. It has been widely believed that A${\beta}$ peptide devided from APP causes apoptotic neurotoxicity in AD brain. However, recent evidence suggests that CTl05(carboxy terminal 105 amino acid peptide fragment of APP) may be an important factor causing neurotoxicity in AD. In addition, AD is one of brain degeneration disease. So we studied on herbal medicine that have a relation of brain degeneration. In Oriental Medicine, Jeonmaedan has been used for disease in relation to brain degeneration. As the result of this study, in Jeonmaedan the apoptosis in the nervous system is inhibited, the repair against the degerneration of SK-N-SH cell lines by CT105 expression is promoted. So Jeonmaedan may be beneficial for the treatment of AD.