Dr. Liza Bergkvist earned her B.S. and M.S. in chemical biology followed by a Ph.D. in protein science from Linköping University. While there, her research focused on the role of amyloid proteins in neurological diseases, particularly Alzheimer’s disease. Her thesis work included the characterization of an improved invertebrate model of Alzheimer’s disease and shone light on the correlation and potential beneficial effect of specific proteins that are part of the innate immune system in relation to Alzheimer’s disease. Dr. Bergkvist also established a fly model for the rare systemic amyloid disease, lysozyme amyloidosis, and investigated the role of serum amyloid P component (a universal component of amyloid aggregates) on the aggregation process and proteotoxicity of disease-associated lysozyme variants. In 2018, she joined the lab of Dr. Patrik Brundin at Van Andel Institute as a postdoctoral fellow.
Dr. Bergkvist’s work primarily focuses on repurposing diabetes drugs for the treatment of Parkinson’s disease, an approach that has the potential to get new therapies to patients faster. Specifically, she uses models of Parkinson’s to investigate if combining two anti-diabetic medications will result in synergistic beneficial effects (as have been seen when the combination is used in the treatment of diabetes). As part of her work, she will evaluate the potential disease-modifying properties of the drugs and determine if they could be used in the early stages of Parkinson’s to alter disease progression, something no current medication can do.
As a secondary project, she also investigates if the propagation of a-synuclein pathology is increased as a consequence to exposure to nanoparticles, such as air pollutants
Ph.D. in protein science, Linköping University (Adviser: Associate Professor Ann-Christin Brorsson )
Thesis: Amyloid-beta and lysozyme proteotoxicity in Drosophila
M.S. in chemical biology, Linköping University
B.S. in chemical biology, Linköping University
Volkswagen stiftung (2016)
Gamla Tjänarinnor (2015–2016)
Bergkvist L, Sandin L, Kågedal K, Brorsson AC. 2016. AβPP processing results in greater toxicity per amount of Aβ1-42 than individually expressed and secreted Aβ1-42 in Drosophila melanogaster. Biol Open 5(8):1030–1039.
Helmfors L*, Bergkvist L*, Brorsson AC. 2016. Serum amyloid P component ameliorates neurological damage caused by expressing a lysozyme variant in the central nervous system of Drosophila melanogaster. PLoS One 11(7):e0159294.
Sandin L*, Bergkvist L*, Nath S, Kielkopf C, Janefjord C, Helmfors L, Zetterberg H, Blennow K, Li H, Nilsberth C, Garner B, Brorsson AC, Kågedal K. 2016. Beneficial effects of increased lysozyme levels in Alzheimer’s disease modelled in Drosophila melanogaster. FEBS J 283(19):3508–3522.