The role of mitochondria in Alzheimer’s disease
Mitochondria supply cells with energy, and this function is known to deteriorate in the case of Alzheimer’s disease. Maria Ankarcrona’s research aims to explain why this happens and what the consequences are. The goal is to contribute to new medications to slow the progress of the disease.
What are you researching?
“I research cellular mechanisms in Alzheimer’s disease. More specifically, we study the role of mitochondria in this disease. The fact that their function in nerve cells is impaired in Alzheimer’s and other neurodegenerative diseases is something we have known for a while. This causes reduced energy production in cells, which we believe is important in regard to the progression of the disease. We want to understand why the mitochondria appear not to function properly and how it can be improved. Most of our research is done in cultured nerve cells, but we also do some studies on donated human tissue.”
What do you hope to achieve?
“Our long-term goal is to find new ways to treat Alzheimer’s. If we can postpone the progression of the disease, many people would have a better life into old age. Any treatment used would probably need to fight the disease on several fronts; our contribution in that case would be a substance that enhances mitochondrial function and allows the nerve cells to function longer. In addition to this specific goal, we want to increase knowledge about the role of mitochondria in the cell at a deeper level. They are not only the power plants of the cell, but are also involved in a variety of functions, from calcium balance to programmed cell death, and they interact closely with other parts of the cell, not least the endoplasmic reticulum (ER).”
What are your most important discoveries so far?
“We have shown how the betaamyloid peptide, which forms the plaques typically seen in Alzheimer’s, enters the mitochondrion. This occurs through a specific pore in its membrane. We were also the first to show how mitochondria and the ER interact in nerve cells and how this differs between healthy cells and Alzheimer’s-affected cells.
Recently, we also presented a new function of the TOM70 protein in the interaction between mitochondria and the ER. TOM70 is involved in the transfer of calcium from the ER to mitochondria. This was a previously unknown function and a very exciting discovery.”
Professor of Experimental Neurogeriatrics at the Department of Neurobiology, Care Sciences and Society
Maria Ankarcrona was born in Linköping in 1965. She studied biology and chemistry at Stockholm University and graduated in 1991. In 1996, she completed a PhD in toxicology at Karolinska Institutet with a dissertation on the mechanisms behind programmed cell death, including nerve cells. That same year, she conducted postdoctoral research with Paul Greengard at the Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, USA.
Maria Ankarcrona became an associate professor in 2004. Since 1998, she has been working at the Department of Neurobiology, Care Sciences and Society where she is currently head of the Division of Neurogeriatrics. Maria Ankarcrona was appointed Professor of Experimental Neurogeriatrics at Karolinska Institutet on 24 May 2018.
Text: Anders Nilsson, first published in "From Cell to Society" 2018