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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/5345578
- author
- Blennow, Kaj
LU
; Mattsson, Niklas
LU
; Schöll, Michael
; Hansson, Oskar
LU
and Zetterberg, Henrik
LU
- organization
- publishing date
- 2015
- 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
- pmid:25840462
- scopus:84937758712
- 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
- 2016-04-01 10:25:12
- date last changed
- 2023-12-08 17:59:44
@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}},
doi = {{10.1016/j.tips.2015.03.002}},
volume = {{36}},
year = {{2015}},
}