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Amyloid-beta 1-40 is associated with alterations in NG2+ pericyte population ex vivo and in vitro
Umeå University, Faculty of Medicine, Department of Medical Biochemistry and Biophysics.
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2018 (English)In: Aging Cell, ISSN 1474-9718, E-ISSN 1474-9726, Vol. 17, no 3, article id e12728Article in journal (Refereed) Published
Abstract [en]

The population of brain pericytes, a cell type important for vessel stability and blood brain barrier function, has recently been shown altered in patients with Alzheimer's disease (AD). The underlying reason for this alteration is not fully understood, but progressive accumulation of the AD characteristic peptide amyloid-beta (Aβ) has been suggested as a potential culprit. In the current study, we show reduced number of hippocampal NG2+ pericytes and an association between NG2+ pericyte numbers and Aβ1-40 levels in AD patients. We further demonstrate, using in vitro studies, an aggregation-dependent impact of Aβ1-40 on human NG2+ pericytes. Fibril-EP Aβ1-40 exposure reduced pericyte viability and proliferation and increased caspase 3/7 activity. Monomer Aβ1-40 had quite the opposite effect: increased pericyte viability and proliferation and reduced caspase 3/7 activity. Oligomer-EP Aβ1-40 had no impact on either of the cellular events. Our findings add to the growing number of studies suggesting a significant impact on pericytes in the brains of AD patients and suggest different aggregation forms of Aβ1-40 as potential key regulators of the brain pericyte population size.

Place, publisher, year, edition, pages
John Wiley & Sons, 2018. Vol. 17, no 3, article id e12728
Keywords [en]
Alzheimer's disease, amyloid-beta 1-40, hippocampus, pericytes
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:umu:diva-148051DOI: 10.1111/acel.12728ISI: 000431962300002PubMedID: 29453790OAI: oai:DiVA.org:umu-148051DiVA, id: diva2:1218108
Note

Listed as co-author in the publication: The Netherlands Brain Bank, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands

Available from: 2018-06-14 Created: 2018-06-14 Last updated: 2018-06-14Bibliographically approved

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Brännström, KristofferOlofsson, Anders
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