Biochemical diagnostic markers to detect early Alzheimer's disease

被引：5

作者：

Lannfelt, L ^{[1
]}

机构：

[1] Huddinge Hosp, Karolinska Inst, Dept Clin Neurosci Geriatr Med, S-14186 Huddinge, Sweden

来源：

NEUROBIOLOGY OF AGING | 1998年 / 19卷 / 02期

关键词：

D O I：

10.1016/S0197-4580(98)00012-8

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

引用

页码：165 / 167

页数：3

共 21 条

[1] Cerebrospinal fluid levels of alpha-secretase-cleaved soluble amyloid precursor protein mirror cognition in a Swedish family with Alzheimer disease and a gene mutation [J].

Almkvist, O ;

Basun, H ;

Wagner, SL ;

Rowe, BA ;

Wahlund, LO ;

Lannfelt, L .

ARCHIVES OF NEUROLOGY, 1997, 54 (05) :641-644

[2] A LARGE SWEDISH FAMILY WITH ALZHEIMERS-DISEASE WITH A CODON-670/671 AMYLOID PRECURSOR PROTEIN MUTATION - A CLINICAL AND GENEALOGICAL INVESTIGATION [J].

AXELMAN, K ;

BASUN, H ;

WINBLAD, B ;

LANNFELT, L .

ARCHIVES OF NEUROLOGY, 1994, 51 (12) :1193-1197

[3] Increasing cerebrospinal fluid tau levels in a subgroup of Alzheimer patients with apolipoprotein E allele epsilon 4 during 14 months follow-up [J].

Blomberg, M ;

Jensen, M ;

Basun, H ;

Lannfelt, L ;

Wahlund, LO .

NEUROSCIENCE LETTERS, 1996, 214 (2-3) :163-166

[4] RELEASE OF EXCESS AMYLOID BETA-PROTEIN FROM A MUTANT AMYLOID BETA-PROTEIN PRECURSOR [J].

CAI, XD ;

GOLDE, TE ;

YOUNKIN, SG .

SCIENCE, 1993, 259 (5094) :514-516

[5] EXCESSIVE PRODUCTION OF AMYLOID BETA-PROTEIN BY PERIPHERAL CELLS OF SYMPTOMATIC AND PRESYMPTOMATIC PATIENTS CARRYING THE SWEDISH FAMILIAL ALZHEIMER-DISEASE MUTATION [J].

CITRON, M ;

VIGOPELFREY, C ;

TEPLOW, DB ;

MILLER, C ;

SCHENK, D ;

JOHNSTON, J ;

WINBLAD, B ;

VENIZELOS, N ;

LANNFELT, L ;

SELKOE, DJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (25) :11993-11997

[6] MUTATION OF THE BETA-AMYLOID PRECURSOR PROTEIN IN FAMILIAL ALZHEIMERS-DISEASE INCREASES BETA-PROTEIN PRODUCTION [J].

CITRON, M ;

OLTERSDORF, T ;

HAASS, C ;

MCCONLOGUE, L ;

HUNG, AY ;

SEUBERT, P ;

VIGOPELFREY, C ;

LIEBERBURG, I ;

SELKOE, DJ .

NATURE, 1992, 360 (6405) :672-674

[7] THE STRUCTURE OF THE PRESENILIN-1 (S182) GENE AND IDENTIFICATION OF 6 NOVEL MUTATIONS IN EARLY-ONSET AD FAMILIES [J].

CLARK, RF ;

HUTTON, M ;

FULDNER, RA ;

FROELICH, S ;

KARRAN, E ;

TALBOT, C ;

CROOK, R ;

LENDON, C ;

PRIHAR, G ;

HE, C ;

KORENBLAT, K ;

MARTINEZ, A ;

WRAGG, M ;

BUSFIELD, F ;

BEHRENS, MI ;

MYERS, A ;

NORTON, J ;

MORRIS, J ;

MEHTA, N ;

PEARSON, C ;

LINCOLN, S ;

BAKER, M ;

DUFF, K ;

ZEHR, C ;

PEREZTUR, J ;

HOULDEN, H ;

RUIZ, A ;

OSSA, J ;

LOPERA, F ;

ARCOS, M ;

MADRIGAL, L ;

COLLINGE, J ;

HUMPHREYS, C ;

ASHWORTH, A ;

SARNER, S ;

FOX, N ;

HARVEY, R ;

KENNEDY, A ;

ROQUES, P ;

CLINE, RT ;

PHILLIPS, CA ;

VENTER, JC ;

FORSELL, L ;

AXELMAN, K ;

LILIUS, L ;

JOHNSTON, J ;

COWBURN, R ;

VIITANEN, M ;

WINBLAD, B ;

KOSIK, K .

NATURE GENETICS, 1995, 11 (02) :219-222

[8] Amyloid, the presenilins and Alzheimer's disease [J].

Hardy, J .

TRENDS IN NEUROSCIENCES, 1997, 20 (04) :154-159

[9] INCREASED CEREBROSPINAL-FLUID TAU IN PATIENTS WITH ALZHEIMERS-DISEASE [J].

JENSEN, M ;

BASUN, H ;

LANNFELT, L .

NEUROSCIENCE LETTERS, 1995, 186 (2-3) :189-191

[10]

JENSEN M, 1997, SOC NEUR ABSTR

← 1 2 3 →