Serum levels of the iron binding protein p97 are elevated in Alzheimer's disease

被引:138
作者
Kennard, ML
Feldman, H
Yamada, T
Jefferies, WA
机构
[1] UNIV BRITISH COLUMBIA, BIOTECHNOL LAB, VANCOUVER, BC V6T 1Z3, CANADA
[2] UNIV BRITISH COLUMBIA, DEPT MED GENET, VANCOUVER, BC V6T 1Z3, CANADA
[3] UNIV BRITISH COLUMBIA, DEPT MICROBIOL & IMMUNOL, VANCOUVER, BC V6T 1Z3, CANADA
[4] UNIV BRITISH COLUMBIA, DEPT ZOOL, VANCOUVER, BC V6T 1Z3, CANADA
[5] UNIV BRITISH COLUMBIA, VANCOUVER HOSP & HLTH SCI CTR, DEPT MED, DIV NEUROL, VANCOUVER, BC V6T 2B5, CANADA
[6] CHIBA UNIV, SCH MED, DEPT NEUROL, CHUO KU, CHIBA 260, JAPAN
关键词
D O I
10.1038/nm1196-1230
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alzheimer's disease is a progressive and incurable disease whose prevalence increases dramatically with age. A biochemical marker for monitoring the onset and progression of the disease would be a valuable tool for disease management. In addition, such a marker might be used as an end point in clinical intervention protocols. Here we provide evidence that the soluble form of the iron binding protein p97 is found in elevated amounts in the serum of Alzheimer's patients compared with healthy controls. This biochemical marker has the potential for identifying subjects afflicted with the disease and possibly for monitoring the onset and longitudinal progression of the disease.
引用
收藏
页码:1230 / 1235
页数:6
相关论文
共 46 条
[21]   DETERMINATION OF AMYLOID BETA-PROTEIN PRECURSORS HARBORING ACTIVE FORM OF PROTEINASE-INHIBITOR DOMAINS IN CEREBROSPINAL-FLUID OF ALZHEIMERS-DISEASE PATIENTS BY TRYPSIN-ANTIBODY SANDWICH ELISA [J].
KITAGUCHI, N ;
TOKUSHIMA, Y ;
OISHI, K ;
TAKAHASHI, Y ;
SHIOJIRI, S ;
NAKAMURA, S ;
TANAKA, S ;
KODAIRA, R ;
ITO, H .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 166 (03) :1453-1459
[22]   CANDIDATE GENE FOR THE CHROMOSOME-1 FAMILIAL ALZHEIMERS-DISEASE LOCUS [J].
LEVYLAHAD, E ;
WASCO, W ;
POORKAJ, P ;
ROMANO, DM ;
OSHIMA, J ;
PETTINGELL, WH ;
YU, CE ;
JONDRO, PD ;
SCHMIDT, SD ;
WANG, K ;
CROWLEY, AC ;
FU, YH ;
GUENETTE, SY ;
GALAS, D ;
NEMENS, E ;
WIJSMAN, EM ;
BIRD, TD ;
SCHELLENBERG, GD ;
TANZI, RE .
SCIENCE, 1995, 269 (5226) :973-977
[23]   ALUMINUM, IRON, AND ZINC IONS PROMOTE AGGREGATION OF PHYSIOLOGICAL CONCENTRATIONS OF BETA-AMYLOID PEPTIDE [J].
MANTYH, PW ;
GHILARDI, JR ;
ROGERS, S ;
DEMASTER, E ;
ALLEN, CJ ;
STIMSON, ER ;
MAGGIO, JE .
JOURNAL OF NEUROCHEMISTRY, 1993, 61 (03) :1171-1174
[24]  
MCKHANN G, 1984, NEUROLOGY, V34, P939, DOI 10.1212/WNL.34.7.939
[25]   INTRAMUSCULAR DESFERRIOXAMINE IN PATIENTS WITH ALZHEIMERS-DISEASE [J].
MCLACHLAN, DRC ;
DALTON, AJ ;
KRUCK, TPA ;
BELL, MY ;
SMITH, WL ;
KALOW, W ;
ANDREWS, DF .
LANCET, 1991, 337 (8753) :1304-1308
[26]   REDUCTION OF BETA-AMYLOID PEPTIDE(42), IN THE CEREBROSPINAL-FLUID OF PATIENTS WITH ALZHEIMERS-DISEASE [J].
MOTTER, R ;
VIGOPELFREY, C ;
KHOLODENKO, D ;
BARBOUR, R ;
JOHNSONWOOD, K ;
GALASKO, D ;
CHANG, L ;
MILLER, B ;
CLARK, C ;
GREEN, R ;
OLSON, D ;
SOUTHWICK, P ;
WOLFERT, R ;
MUNROE, B ;
LIEBERBURG, I ;
SEUBERT, P ;
SCHENK, D .
ANNALS OF NEUROLOGY, 1995, 38 (04) :643-648
[27]   The amyloid precursor protein of Alzheimer's disease in the reduction of copper(II) to copper(I) [J].
Multhaup, G ;
Schlicksupp, A ;
Hesse, L ;
Beher, D ;
Ruppert, T ;
Masters, CL ;
Beyreuther, K .
SCIENCE, 1996, 271 (5254) :1406-1409
[28]   A MUTATION IN THE AMYLOID PRECURSOR PROTEIN ASSOCIATED WITH HEREDITARY ALZHEIMERS-DISEASE [J].
MURRELL, J ;
FARLOW, M ;
GHETTI, B ;
BENSON, MD .
SCIENCE, 1991, 254 (5028) :97-99
[29]   AMYLOID-BETA PROTEIN-LEVELS IN CEREBROSPINAL-FLUID ARE ELEVATED IN EARLY-ONSET ALZHEIMERS-DISEASE [J].
NAKAMURA, T ;
SHOJI, M ;
HARIGAYA, Y ;
WATANABE, M ;
HOSODA, K ;
CHEUNG, TT ;
SHAFFER, LM ;
GOLDE, TE ;
YOUNKIN, LH ;
YOUNKIN, SG ;
HIRAI, S .
ANNALS OF NEUROLOGY, 1994, 36 (06) :903-911
[30]   SOLUBLE DERIVATIVES OF THE BETA-AMYLOID PROTEIN-PRECURSOR IN CEREBROSPINAL-FLUID - ALTERATIONS IN NORMAL AGING AND IN ALZHEIMERS-DISEASE [J].
PALMERT, MR ;
USIAK, M ;
MAYEUX, R ;
RASKIND, M ;
TOURTELLOTTE, WW ;
YOUNKIN, SG .
NEUROLOGY, 1990, 40 (07) :1028-1034