Amyloid-β1–43 cerebrospinal fluid levels and the interpretation of APP, PSEN1 and PSEN2 mutations

被引：0
作者：
Federica Perrone
Maria Bjerke
Elisabeth Hens
Anne Sieben
Maarten Timmers
Arne De Roeck
Rik Vandenberghe
Kristel Sleegers
Jean-Jacques Martin
Peter P. De Deyn
Sebastiaan Engelborghs
Julie van der Zee
Christine Van Broeckhoven
Rita Cacace
机构：
[1] Neurodegenerative Brain Diseases Group,Department of Biomedical Sciences
[2] VIB Center for Molecular Neurology,Reference Centre for Biological Markers of Dementia (BIODEM), Institute Born
[3] Institute Born-Bunge,Bunge
[4] University of Antwerp,Laboratory of Neurochemistry and Center for Neurosciences
[5] University of Antwerp,Department of Neurology and Memory Clinic
[6] UZ Brussel and Vrije Universiteit Brussel,Department of Neurology
[7] Hospital Network Antwerp,Department of Neurology
[8] Middelheim and Hoge Beuken,Department of Neurology
[9] University Hospital Antwerp,Department of Neurosciences, Faculty of Medicine
[10] University Hospital Brussel and Center for Neurosciences,Laboratory of Cognitive Neurology, Department of Neurology
[11] Vrije Universiteit Brussel,undefined
[12] University Hospital Ghent and University of Ghent,undefined
[13] Janssen Research and Development,undefined
[14] Division of Janssen Pharmaceutica NV,undefined
[15] KU Leuven,undefined
[16] University Hospitals Leuven,undefined
来源：
Alzheimer's Research & Therapy | / 12卷
关键词：
Alzheimer’s disease (AD); Amyloid-β 1–43 (Aβ; ); Cerebrospinal fluid (CSF); Alzheimer mutations; Oxford Nanopore Technologies (ONT) long-read sequencing;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
引用
收藏
相关论文
共 251 条
[11]  
Saito T(2012)Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans Arch Gen Psychiatry 69 98-870
[12]  
Saido TC(2016)Cerebrospinal fluid levels ofβ-amyloid 1–42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia Front Aging Neurosci 8 30-1032
[13]  
Chávez-Gutiérrez L(2014)Cerebrospinal fluid levels of amyloid beta 1–43 in patients with amnestic mild cognitive impairment or early Alzheimer’s disease: a 2-year follow-up study Acta Neuropathol Commun 2 135-706
[14]  
De Strooper B(1996)Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer’s disease Nat Med 2 864-456.e14
[15]  
Hyman BT(2011)Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer’s disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer’s disease Nat Neurosci 14 1023-1344
[16]  
Phelps CH(2009)Potent amyloidogenicity and pathogenicity of Aβ43 J Neurochem 110 697-269
[17]  
Beach TG(2019)Aβ43 is more frequent than Aβ40 in amyloid plaque cores from Alzheimer disease brains Acta Neuropathol Commun 7 141-699
[18]  
Bigio EH(2013)Aβ43 in human Alzheimer’s disease: effects of active Aβ42 immunization PLoS One 8 55847-1449
[19]  
Cairns NJ(2017)The pathogenic Ab43 is enriched in familial and sporadic Alzheimer disease Cell 170 443-442
[20]  
Carrillo MC(2012)Alzheimer’s-causing mutations shift Aβ length by destabilizing γ-secretase-Aβn interactions Hum Mutat 33 1340-2983
12345678910