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Unraveling the molecular pathway of Alzheimer's disease: research about presenilins gathers momentum.

作者信息

Sandbrink R, Beyreuther K

机构信息

Central Institute for Mental Health, Mannheim, Germany,

出版信息

Mol Psychiatry. 1996 Dec;1(6):438-44.

PMID:9154244
Abstract

Missense mutations of the presenilins (PS1 and PS2) first identified about one year ago are responsible for the majority of autosomal dominant familial Alzheimer's disease cases. Recent studies suggesting that these mutations exert their disastrous effect by elevating the levels of the longer form of beta-amyloid (A beta 42) are reviewed.

摘要

相似文献

1
Unraveling the molecular pathway of Alzheimer's disease: research about presenilins gathers momentum.
Mol Psychiatry. 1996 Dec;1(6):438-44.
2
Presenilins and early-onset familial Alzheimer's disease.
Neuroreport. 1997 May 27;8(8):i-xii.
3
[From gene to disease; presenilins and Alzheimer disease].
Ned Tijdschr Geneeskd. 2001 Oct 20;145(42):2027-9.
4
Presenilins and Alzheimer's disease: the role of A beta 42.早老素与阿尔茨海默病:β淀粉样蛋白42的作用
J Neural Transm Suppl. 1998;53:181-4.
5
Presenilin 2 familial Alzheimer's disease mutations result in partial loss of function and dramatic changes in Abeta 42/40 ratios.早老素2家族性阿尔茨海默病突变导致功能部分丧失以及β淀粉样蛋白42/40比率发生显著变化。
J Neurochem. 2005 Jan;92(2):294-301. doi: 10.1111/j.1471-4159.2004.02858.x.
6
[Genetic factors in the pathogenesis of Alzheimer's disease: roles of beta-amyloid and presenilins].
Tanpakushitsu Kakusan Koso. 1998 Oct;43(13):1963-72.
7
[Presenilins as a marker of Alzheimer's disease].[早老素作为阿尔茨海默病的标志物]
Ned Tijdschr Geneeskd. 1998 May 30;142(22):1247-52.
8
Presenilin mutations in Alzheimer's disease.阿尔茨海默病中的早老素突变
Hum Mutat. 1998;11(3):183-90. doi: 10.1002/(SICI)1098-1004(1998)11:3<183::AID-HUMU1>3.0.CO;2-J.
9
[Molecular genetics of Alzheimer's disease--presenilin and other genes].[阿尔茨海默病的分子遗传学——早老素及其他基因]
Rinsho Shinkeigaku. 1997 Dec;37(12):1095-6.
10
Mapping the APP/presenilin (PS) binding domains: the hydrophilic N-terminus of PS2 is sufficient for interaction with APP and can displace APP/PS1 interaction.绘制淀粉样前体蛋白(APP)/早老素(PS)结合结构域:PS2的亲水性N末端足以与APP相互作用,并可取代APP/PS1的相互作用。
Neurobiol Dis. 1999 Feb;6(1):43-55. doi: 10.1006/nbdi.1998.0212.

引用本文的文献

1
Vaccination strategies for Alzheimer's disease: A new hope?阿尔茨海默病的疫苗接种策略:新希望?
Drugs Aging. 2007;24(2):107-19. doi: 10.2165/00002512-200724020-00003.
2
Does beta-amyloid plaque formation cause structural injury to neuronal processes?β-淀粉样蛋白斑块的形成会对神经突造成结构损伤吗?
Neurotox Res. 2005;7(1-2):5-15. doi: 10.1007/BF03033772.
3
Beta-amyloid and cholinergic neurons.β-淀粉样蛋白与胆碱能神经元。
Neurochem Res. 2003 Apr;28(3-4):499-506. doi: 10.1023/a:1022865121743.