Rapidly Progressive Alzheimer's Disease: A Multicenter Update

被引：45

作者：

Schmidt, Christian ^{[1
]}

Haik, Stephane ^{[2
,3
,4
,5
,7
]}

Satoh, Katsuya ^{[14
]}

Rabano, Alberto ^{[8
,9
]}

Martinez-Martin, Pablo ^{[8
,9
]}

Roeber, Sigrun ^{[13
]}

Brandel, Jean-Philippe ^{[2
,3
,4
,5
]}

Calero-Lara, Miguel ^{[11
,12
]}

de Pedro-Cuesta, Jesus ^{[10
,11
]}

Laplanche, Jean-Louis ^{[6
]}

Hauw, Jean-Jaques ^{[7
]}

Kretzschmar, Hans ^{[13
]}

Zerr, Inga ^{[1
]}

机构：

[1] Univ Gottingen, Dept Neurol, Natl Reference Ctr TSE Surveillance, D-3400 Gottingen, Germany

[2] Grp Hosp Pitie Salpetriere, AP HP, F-75634 Paris, France

[3] Univ Paris 06, Ctr Rech, Inst Cerveau & Moelle Epiniere, UMR S975, Paris, France

[4] INSERM, U975, Paris, France

[5] CNRS, UMR 7225, Paris, France

[6] Hop Lariboisiere, AP HP, Serv Biochim & Biol Mol, F-75475 Paris, France

[7] Grp Hosp Pitie Salpetriere, Lab Neuropathol Raymond Escourolle, F-75634 Paris, France

[8] Carlos III Inst Hlth, Res Unit, Alzheimer Ctr Reina Sofia Fdn, Madrid, Spain

[9] Carlos III Inst Hlth, CIEN Fdn, CIBERNED, Madrid, Spain

[10] Carlos III Inst Hlth, Natl Ctr Epidemiol, Madrid, Spain

[11] Carlos III Inst Hlth, CIBERNED, Madrid, Spain

[12] Carlos III Inst Hlth, Natl Ctr Microbiol, Madrid, Spain

[13] Univ Munich, Dept Neuropathol, Munich, Germany

[14] Nagasaki Univ, Grad Sch Biomed Sci, Dept Mol Microbiol & Immunol, Nagasaki 852, Japan

来源：

JOURNAL OF ALZHEIMERS DISEASE | 2012年 / 30卷 / 04期

关键词：

Alzheimer's disease; heterogeneity; rapid decline; CREUTZFELDT-JAKOB-DISEASE; PRION PROTEIN; ASSOCIATION; DIAGNOSIS;

D O I：

10.3233/JAD-2012-120007

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The objective was to characterize a rapidly progressive subtype of Alzheimer's disease (rpAD). Multicenter (France, Germany, Japan, Spain) retrospective analyses of neuropathologically confirmed rpAD cases initially classified as prion disease due to their clinical phenotype were performed. Genetic properties, cerebrospinal fluid biomarkers, neuropathology, and clinical features were examined. Eighty-nine patients were included (median survival 10 months). APOE and PRNP codon 129 genotype distribution paralleled a healthy control group. APOE epsilon 4 homozygosity was absent. Cerebrospinal fluid biomarkers were abnormal, but within a range as expected for classic AD, except for proteins 14-3-3, which were detectable in 42%. Thus, evidence of the existence of rpAD is accumulating. The APOE profile is intriguing, suggesting that this very rapid disease form might represent a distinct subtype of Alzheimer's disease.

引用

页码：751 / 756

页数：6

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