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Erschienen in: Journal of Neural Transmission 2/2018

01.12.2017 | High Impact Review in Neuroscience, Neurology or Psychiatry - Review Article

Amyloid β oligomers (AβOs) in Alzheimer’s disease

verfasst von: Barbara Mroczko, Magdalena Groblewska, Ala Litman-Zawadzka, Johannes Kornhuber, Piotr Lewczuk

Erschienen in: Journal of Neural Transmission | Ausgabe 2/2018

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Abstract

The causative role of amyloid β 1–42 (Aβ42) aggregation in the pathogenesis of Alzheimer’s disease (AD) has been under debate for over 25 years. Primarily, scientific efforts have focused on the dyshomeostasis between production and clearance of Aβ42. This imbalance may result from mutations either in genes for the substrate, i.e., amyloid precursor protein or in genes encoding presenilin, the enzyme of the reaction that generates Aβ42. Currently, it is supposed that soluble oligomers of amyloid beta (AβOs) and not fibrillar Aβ42 within neuritic plaques may be the toxic factors acting on a very early stage of AD, perhaps even initiating pathological cascade. For example, soluble AβOs isolated from AD patients’ brains reduced number of synapses, inhibited long-term potentiation, and enhanced long-term synaptic depression in brain regions responsible for memory in animal models of AD. Concentrations of AβOs in the cerebrospinal fluid (CSF) of AD patients are often reported higher than in non-demented controls, and show a negative correlation with mini-mental state examination scores. Furthermore, increased Aβ42/oligomer ratio in the CSF of AD/MCI patients indicated that the presence of soluble AβOs in CSF may be linked to lowering of natively measured monomeric Aβ42 by epitopes masking, and hence, concentrations of AβOs in the CSF are postulated to as useful AD biomarkers.
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Metadaten
Titel
Amyloid β oligomers (AβOs) in Alzheimer’s disease
verfasst von
Barbara Mroczko
Magdalena Groblewska
Ala Litman-Zawadzka
Johannes Kornhuber
Piotr Lewczuk
Publikationsdatum
01.12.2017
Verlag
Springer Vienna
Erschienen in
Journal of Neural Transmission / Ausgabe 2/2018
Print ISSN: 0300-9564
Elektronische ISSN: 1435-1463
DOI
https://doi.org/10.1007/s00702-017-1820-x

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