Lithium ions display weak interaction with amyloid-beta (Aβ) peptides and have minor effects on their aggregation

Elina Berntsson; Suman Paul; Faraz Vosough; Sabrina B. Sholts; Jüri Jarvet; Per M. Roos; Andreas  Barth; Astrid Gräslund; Sebastian Wärmländer

doi:10.18388/abp.2020_5493

Elina Berntsson 1Department of Biochemistry and Biophysics, Stockholm University, Sweden; 2Department of Chemistry and Biotechnology, Tallinn University of Technology, Estonia
Suman Paul Department of Biochemistry and Biophysics, Stockholm University, Sweden
Faraz Vosough Department of Biochemistry and Biophysics, Stockholm University, Sweden
Sabrina B. Sholts Department of Biochemistry and Biophysics, Stockholm University, Sweden
Jüri Jarvet 1Department of Biochemistry and Biophysics, Stockholm University, Sweden; 2The National Institute of Chemical Physics and Biophysics, Tallinn, Estonia
Per M. Roos 1Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; 2Department of Clinical Physiology, Capio St. Göran Hospital, Stockholm, Sweden
Andreas Barth Department of Biochemistry and Biophysics, Stockholm University, Sweden
Astrid Gräslund Department of Biochemistry and Biophysics, Stockholm University, Sweden
Sebastian Wärmländer Department of Biochemistry and Biophysics, Stockholm University, Sweden

DOI: https://doi.org/10.18388/abp.2020_5493

Abstract

Alzheimer’s disease (AD) is an incurable disease and the main cause of age-related dementia worldwide, despite decades of research. Treatment of AD with lithium (Li) has showed promising results, but the underlying mechanism is unclear. The pathological hallmark of AD brains is deposition of amyloid plaques, consisting mainly of amyloid-β (Aβ) peptides aggregated into amyloid fibrils. The plaques contain also metal ions of e.g. Cu, Fe, and Zn, and such ions are known to interact with Aβ peptides and modulate their aggregation and toxicity. The interactions between Aβ peptides and Li+ ions have however not been well investigated. Here, we use a range of biophysical techniques to characterize in vitro interactions between Aβ peptides and Li+ ions. We show that Li+ ions display weak and non-specific interactions with Aβ peptides, and have minor effects on Aβ aggregation. These results indicate that possible beneficial effects of Li on AD pathology are not likely caused by direct interactions between Aβ peptides and Li+ ions.