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Trends Pharmacol Sci. 2015 May;36(5):297-309. doi: 10.1016/j.tips.2015.03.002. Epub 2015 Apr 1.

Amyloid biomarkers in Alzheimer's disease.

Author information

1
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; The Torsten Söderberg Professorship at the Royal Swedish Academy of Sciences. Electronic address: kaj.blennow@neuro.gu.se.
2
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA; Department of Radiology and Biomedical Imaging, University of California, San Francisco, CA, USA.
3
Helen Wills Neuroscience Institute, University of California, Berkeley, CA, USA; Department of Clinical Neuroscience and Rehabilitation, University of Gothenburg, Gothenburg, Sweden.
4
Department of Clinical Sciences, Lund University, Lund, Sweden; Clinical Memory Research unit, Clinical Sciences, Lund University, Lund, Sweden.
5
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; UCL Institute of Neurology, Queen Square, London, UK.

Abstract

Aggregation of amyloid-β (Aβ) into oligomers, fibrils, and plaques is central in the molecular pathogenesis of Alzheimer's disease (AD), and is the main focus of AD drug development. Biomarkers to monitor Aβ metabolism and aggregation directly in patients are important for further detailed study of the involvement of Aβ in disease pathogenesis and to monitor the biochemical effect of drugs targeting Aβ in clinical trials. Furthermore, if anti-Aβ disease-modifying drugs prove to be effective clinically, amyloid biomarkers will be of special value in the clinic to identify patients with brain amyloid deposition at risk for progression to AD dementia, to enable initiation of treatment before neurodegeneration is too severe, and to monitor drug effects on Aβ metabolism or pathology to guide dosage. Two types of amyloid biomarker have been developed: Aβ-binding ligands for use in positron emission tomography (PET) and assays to measure Aβ42 in cerebrospinal fluid (CSF). In this review, we present the rationales behind these biomarkers and compare their ability to measure Aβ plaque load in the brain. We also review possible shortcomings and the need of standardization of both biomarkers, as well as their implementation in the clinic.

KEYWORDS:

Alzheimer's disease; biomarker; cerebrospinal fluid; positron emission tomography (PET); β-amyloid (Aβ)

PMID:
25840462
DOI:
10.1016/j.tips.2015.03.002
[Indexed for MEDLINE]

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