• 대한의생명과학회지
• /
• 제26권1호
• /
• pp.1-7
• /
• 2020

Alzheimer's disease (AD) is the most common neurodegenerative disorder and is expected to become more and more widespread as life expectancy increases. New therapeutic target, as well as the identification of mechanisms responsible for pathology, is urgently needed. Recently, microglial actin cytoskeleton has been proposed as a beneficial role in axon regeneration of brain injury. This review highlights in understanding of the characteristics of microglial actin cytoskeleton and discuss the role of specific actin-interacting proteins and receptors in AD. The precise mechanisms and functional aspects of motility by microglia require further study, and the regulation of microglial actin cytoskeleton might be a potential therapeutic strategy for neurological diseases.

• 생물정신의학
• /
• 제17권4호
• /
• pp.194-202
• /
• 2010

Alzheimer's disease(AD) is the most common neurodegenerative disorder and constitutes about two thirds of dementia. Despite a lot of effort to find drugs for AD worldwide, an efficient medicine that can cure AD has not come yet, which is due to the complicated pathogenic pathways and progressively degenerative properties of AD. In its early clinical phase, it is important to find the subtle alterations in synapses responsible for memory because symptoms of AD patients characteristically start with pure impairment of memory. Attempts to find the target synaptic proteins and their pathogenic pathways will be the most powerful alternative strategy for developing AD medicine. Here we review recent progress in deciphering the role of target synaptic proteins related to AD in hippocampal glutamatergic synapses.

• BMB Reports
• /
• 제53권1호
• /
• pp.35-46
• /
• 2020

Despite enduring diverse insults, mitochondria maintain normal functions through mitochondrial quality control. However, the failure of mitochondrial quality control resulting from excess damage and mechanical defects causes mitochondrial dysfunction, leading to various human diseases. Recent studies have reported that mitochondrial defects are found in Alzheimer's disease (AD) and worsen AD symptoms. In AD pathogenesis, mitochondrial dysfunction-driven generation of reactive oxygen species (ROS) and their contribution to neuronal damage has been widely studied. In contrast, studies on mitochondrial dysfunction-associated inflammatory responses have been relatively scarce. Moreover, ROS produced upon failure of mitochondrial quality control may be linked to the inflammatory response and influence the progression of AD. Thus, this review will focus on inflammatory pathways that are associated with and initiated through defective mitochondria and will summarize recent progress on the role of mitochondria-mediated inflammation in AD. We will also discuss how reducing mitochondrial dysfunction-mediated inflammation could affect AD.

• BMB Reports
• /
• 제52권12호
• /
• pp.679-688
• /
• 2019

The decrease of metabolism in the brain has been observed as the important lesions of Alzheimer's disease (AD) from the early stages of diagnosis. The cumulative evidence has reported that the failure of mitochondria, an organelle involved in diverse biological processes as well as energy production, maybe the cause or effect of the pathogenesis of AD. Both amyloid and tau pathologies have an impact upon mitochondria through physical interaction or indirect signaling pathways, resulting in the disruption of mitochondrial function and dynamics which can trigger AD. In addition, mitochondria are involved in different biological processes depending on the specific functions of each cell type in the brain. Thus, it is necessary to understand mitochondrial dysfunction as part of the pathological phenotypes of AD according to each cell type. In this review, we summarize that 1) the effects of AD pathology inducing mitochondrial dysfunction and 2) the contribution of mitochondrial dysfunction in each cell type to AD pathogenesis.

• 대한인간공학회:학술대회논문집
• /
• 대한인간공학회 1996년도 춘계학술대회논문집
• /
• pp.160-167
• /
• 1996

The early diagnosis has an very important role in curing dementia. But there was not an effective method to diagnose it until now. In this paper we analyzed the EEG in Alzheimer's disease and normal control groups to compare by nonlinear parameter such as the largest Lyapunov exponent $L_{1}$. We found that patients with Alzheimer's disease have significantly lower$L_{1}$ than normal groups. And we propose the nonlinear analysis of EEG as a useful tool for the early diagnosis of Alzheimer's disease.

• Bulletin of the Korean Chemical Society
• /
• 제34권5호
• /
• pp.1503-1507
• /
• 2013

The two major symptoms characterizing Alzheimer's disease are the formation of amyloid-${\beta}$ extracellular deposits in the form of senile plaques and intracellular neurofibrillary tangles (NFTs) that consist of pathological hyperphosphorylated tau protein aggregated into insoluble paired helical filaments (PHFs). Neurons of the central nervous system have appreciable amounts of tau protein, a microtubule-associated protein. To maintain an optimal operation of nerves, the microtubules are stabilized, which is necessary to support cell structure and cellular processes. When the modified tau protein becomes dysfunctional, the cells containing misfolded tau cannot maintain cell structure. One of the pathological hallmarks of Alzheimer's disease is hyperphosphorylated tau protein. This paper shows that the small heat shock protein from humans (Hsp27) reduces hyperphosphorylated tau and prevents hyperphosphorylated tau-induced cell death of the human neuroblastoma cell line SH-SY5Y.

• 센서학회지
• /
• 제22권4호
• /
• pp.281-285
• /
• 2013

In this study a biosensor was developed by using Drosophila cells expressing a gustatory receptor Gr5a and an ion sensitive field effect transistors (ISFETs) sensor device, which demonstrated significant compatibility with the Drosophila cells expressing Gr5a and their response to sugar. These results suggested that the newly developed cell based biosensor has a potential as a simple and easy screening device for Alzheimer's disease in the future.

• 대한치매학회지
• /
• 제17권4호
• /
• pp.131-136
• /
• 2018

Alzheimer's disease (AD) related genes have been elucidated by advanced genetic techniques. Familial autosomal dominant AD genes founded by linkage analyses are APP, PSEN1, PSEN2, ABCA7, and SORL1. Genome-wide association studies have found risk genes such as ABCA7, BIN1, CASS4, CD33, CD2AP, CELF1, CLU, CR1, DSG2, EPHA1, FERMT2, HLA-DRB5-HLA-DRB1, INPP5D, MEF2C, MS4A6A/MS4A4E, NME8, PICALM, PTK2B, SLC24A4, SORL1, and ZCWPW1. ABCA7, SORL1, TREM2, and APOE are proved to have high odds ratio (>2) in risk of AD using next generation sequencing studies. Thanks to the promising genetic techniques such as CRISPR-CAS9 and single-cell RNA sequencing opened a new era in genetics. CRISPR-CAS9 can directly link genetic knowledge to future treatment. Single-cell RNA sequencing are providing useful information on cell biology and pathogenesis of diverse diseases.

• 식품저장과 가공산업
• /
• 제6권2호
• /
• pp.25-29
• /
• 2007

Phytochemicals have long been known to hold a number of physiological benefits, including antioxidant, anticardiovascular activities and anticancer. The profitable effects of phytochemicals from food sources such as vegetables and fruits, with respect to neurodegeneration, are only beginning to receive increased attention. Alzheimer's disease(AD) is one of the major neurodegenerative diseases for which no treatment is available, and characterized by loss of cognitiion and memory. Many recent studies show that the brain of AD patient is subjected to increased oxidative stress resulting from free radical damage, and the resulting cellular malfunctions are widely believed to be responsible for neuronal degeneration in AD. In this study, the relative relation between D and phytochemicals were surveyed.

• Genomics & Informatics
• /
• 제18권4호
• /
• pp.39.1-39.8
• /
• 2020

Alzheimer's disease (AD) is a chronic, progressive brain disorder that slowly destroys affected individuals' memory and reasoning faculties, and consequently, their ability to perform the simplest tasks. This study investigated the hub genes of AD. Proteins interact with other proteins and non-protein molecules, and these interactions play an important role in understanding protein function. Computational methods are useful for understanding biological problems, in particular, network analyses of protein-protein interactions. Through a protein network analysis, we identified the following top 10 hub genes associated with AD: PTGER3, C3AR1, NPY, ADCY2, CXCL12, CCR5, MTNR1A, CNR2, GRM2, and CXCL8. Through gene enrichment, it was identified that most gene functions could be classified as integral to the plasma membrane, G-protein coupled receptor activity, and cell communication under gene ontology, as well as involvement in signal transduction pathways. Based on the convergent functional genomics ranking, the prioritized genes were NPY, CXCL12, CCR5, and CNR2.