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Amyloid biomarkers in Alzheimer's disease.

Blennow, Kaj LU ; Mattsson, Niklas LU ; Schöll, Michael; Hansson, Oskar LU and Zetterberg, Henrik LU (2015) In Trends in Pharmacological Sciences 36(5). p.297-309
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... (More)
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. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
Trends in Pharmacological Sciences
volume
36
issue
5
pages
297 - 309
publisher
Elsevier
external identifiers
  • pmid:25840462
  • wos:000355045200005
ISSN
0165-6147
DOI
10.1016/j.tips.2015.03.002
language
English
LU publication?
yes
id
616fe24b-5a73-4dfb-af9f-7863798ac42d (old id 5345578)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25840462?dopt=Abstract
date added to LUP
2015-05-06 16:51:47
date last changed
2016-09-30 05:35:35
@article{616fe24b-5a73-4dfb-af9f-7863798ac42d,
  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.},
  author       = {Blennow, Kaj and Mattsson, Niklas and Schöll, Michael and Hansson, Oskar and Zetterberg, Henrik},
  issn         = {0165-6147},
  language     = {eng},
  number       = {5},
  pages        = {297--309},
  publisher    = {Elsevier},
  series       = {Trends in Pharmacological Sciences},
  title        = {Amyloid biomarkers in Alzheimer's disease.},
  url          = {http://dx.doi.org/10.1016/j.tips.2015.03.002},
  volume       = {36},
  year         = {2015},
}