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알쯔하이머 질환의 신경생물학
논문 개요
| 기관명 | NDSL |
|---|---|
| 저널명 | 생물정신의학 = Korean journal of biological psychiatry |
| ISSN | 1225-8709,2005-7571 |
| ISBN |
논문저자 및 소속기관 정보
| 저자(한글) | 정영조,서승우,이승환 |
|---|---|
| 저자(영문) | |
| 소속기관 | |
| 소속기관(영문) | |
| 출판인 | |
| 간행물 번호 | |
| 발행연도 | 2001-01-01 |
| 초록 | Alzheimer's disease(AD) is associated with a characteristic neuropathology. The major hallmarks of AD are senile plaques (SPs) and neurofibrillary tangles(NFTs). ${ beta}$ -amyloid protein( $A{ beta}$ ) is derived from the proteolysis of amyloid precursor protein(APP) and then converted to SPs. Mature SPs produce cytotoxicity through direct toxic effects and activation of microglia and complement. NFTs are composed of paired helical filaments(PHFs) including abnormally phosphorylated form of the microtubule-associated protein(MAP) tau and increased tau level in cerebrospinal fluid may be observed in most AD. The aggregation of $A{ beta}$ and tau formation are thought to be a final common pathway of AD. Acetylcholine, dopamine, serotonin, GABA and their receptors are associated with AD. Especially, decreased nicotinic acetylcholine receptors(nAChRs) in AD are reported. Genetic lesions associated with AD are mutations in the structural genes for the APP located on chromosome 21, presenilin(PSN)1 located on chromosome 14 and PSN2 located on chromosome 1. Also, trisomy 21, Apo-E gene located on chromosome 19, PMF locus, low density lipoprotein receptor-related protein and ${ alpha}$ -macroglobulin increase risk of AD. In this article, we will review about the neurobiology of AD and some newly developed research areas. |
| 원문URL | http://click.ndsl.kr/servlet/OpenAPIDetailView?keyValue=03553784&target=NART&cn=JAKO200135164626861 |
| 첨부파일 |
추가정보
| 과학기술표준분류 | |
|---|---|
| ICT 기술분류 | |
| DDC 분류 | |
| 주제어 (키워드) | 알쯔하이머 질환, lt,TEX gt,${ beta}$ lt,/TEX gt,아밀로이드 단백질,tau 단백질,유전학,Alzheimer's disease, lt,TEX gt,${ beta}$ lt,/TEX gt,-amyloid protein,MAP tau,Genetics |