Abstract
This paper gives a short review on cerebrospinal fluid (CSF) biomarkers for Alzheimer's disease (AD), from early developments to high-precision validated assays on fully automated lab analyzers. We also discuss developments on novel biomarkers, such as synaptic proteins and Aβ oligomers. Our vision for the future is that assaying a set of biomarkers in a single CSF tube can monitor the whole spectrum of AD molecular pathogenic events. CSF biomarkers will have a central position not only for clinical diagnosis, but also for the understanding of the sequence of molecular events in the pathogenic process underlying AD and as tools to monitor the effects of novel drug candidates targeting these different mechanisms.
Highlights
Early Assay DevelopmentsThe story on modern Alzheimer’s disease (AD) biomarker development started in 1995 with a series of publications on enzyme-linked immunosorbent assays (ELISA) based on monoclonal antibodies to measure cerebrospinal fluid (CSF) levels of total tau (T-tau) and phosphorylated tau (P-tau) and the 42 amino acid isoform (Aβ42)
Clinical Neurochemistry Laboratory, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska University Hospital, The Sahlgrenska Academy at University of Specialty section: This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
The Alzheimer’s disease (AD) arena is in the good situation that a set of highly validated and specific biomarkers are at hand; in addition to amyloid positron emission tomography (PET) and magnetic resonance imaging (MRI) measurements, a set of cerebrospinal fluid (CSF) tests reflecting key aspects of disease pathology are available
Summary
The story on modern AD biomarker development started in 1995 with a series of publications on enzyme-linked immunosorbent assays (ELISA) based on monoclonal antibodies to measure CSF levels of total tau (T-tau) and phosphorylated tau (P-tau) and the 42 amino acid isoform (Aβ42). The following years, many research reports consistently showed that the “AD profile” of increased CSF levels of T-tau and P-tau together with decreased Aβ42 had high sensitivity and specificity, both in the range of 85–90%, to identify AD dementia, for review see (Blennow and Hampel, 2003). Since these three CSF biomarkers reflect key elements of AD pathophysiology, i.e., neuronal degeneration (Ttau), tau pathology (P-tau), and amyloid plaques (Aβ42), they are often termed the “core” AD biomarkers (Hampel et al, 2004)
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