The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Cerebrospinal fluid profiles of amyloid β-related biomarkers in Alzheimer's disease.
Christoffer Rosén; Ulf Andreasson; Niklas Mattsson; Jan Marcusson; Lennart Minthon; Niels Andreasen; Kaj Blennow; Henrik Zetterberg (Profiled Author: Blennow, Kaj)
Clinical Neurochemistry Laboratory, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Neuromolecular medicine 2012;14(1):65-73.
The amyloid cascade hypothesis on the pathogenesis of Alzheimer's disease (AD) states that amyloid β (Aβ) accumulation in the brain is a key factor that initiates the neurodegenerative process. Aβ is generated from amyloid precursor protein (APP) through sequential cleavages by BACE1 (the major β-secretase in the brain) and γ-secretase. The purpose of this study was to characterize APP metabolism in vivo in AD patients versus cognitively healthy subjects by examining alterations in cerebrospinal fluid (CSF) biomarkers. We measured BACE1 activity and concentrations of α- and β-cleaved soluble APP (sAPPα and sAPPβ, respectively) and Aβ40 in CSF, biomarkers that all reflect the metabolism of APP, in 75 AD patients and 65 cognitively healthy controls. These analytes were also applied in a multivariate model to determine whether they provided any added diagnostic value to the core CSF AD biomarkers Aβ42, T-tau, and P-tau. We found no significant differences in BACE1 activity or sAPPα, sAPPβ, and Aβ40 concentrations between AD patients and controls. A multivariate model created with all analytes did not improve the separation of AD patients from controls compared with using the core AD biomarkers alone, highlighting the strong diagnostic performance of Aβ42, T-tau, and P-tau for AD. However, AD patients in advanced clinical stage, as determined by low MMSE score (≤20), had lower BACE1 activity and sAPPα, sAPPβ, and Aβ40 concentrations than patients with higher MMSE score, suggesting that these markers may be related to the severity of the disease.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
GANDY, SAMUEL E
15 September 2010 - 30 June 2014
NATIONAL CENTER FOR COMPLEMENTARY &ALTERNATIVE MEDICINE
Total Funding: $ 241,601
GOATE, ALISON M
1 September 2010 - 31 August 2015
NATIONAL INSTITUTE ON AGING
Total Funding: $ 972,692
Golde, Todd E
10 April 2000 - 30 April 2009
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Total Funding: $ 2,532,291
Thor D Stein; Nicholas J Anders; Charles DeCarli; Sic L Chan; Mark P Mattson; Jeffrey A Johnson
Neutralization of transthyretin reverses the neuroprotective effects of secreted amyloid precursor protein (APP) in APPSW mice resulting in tau phosphorylation and loss of hippocampal neurons: support for the amyloid hypothesis.The Journal of neuroscience : the official journal of the Society for Neuroscience 2004;24(35):7707-17.
Sandra D Mulder; Wiesje M van der Flier; Jan H Verheijen; Cees Mulder; Philip Scheltens; Marinus A Blankenstein; C Erik Hack; Robert VeerhuisJournal of Alzheimer's disease : JAD 2010;20(1):253-60.
Michael Ewers; Xin Cheng; Zhenyu Zhong; Hikmet F Nural; Cathal Walsh; Thomas Meindl; Stefan J Teipel; Katharina Buerger; Ping He; Yong Shen; et al.Journal of Alzheimer's disease : JAD 2011;25(2):373-81.
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