Astrocytes in Alzheimer's and Parkinson's disease

Members of the group

Anna Erlandsson, Associate Professor, PhD
Jinar Rostami, PhD
Chiara Beretta, PhD-student
Tobias Mothes, PhD-student
Abdulkhalek Dakhel, PhD-student
Khalid Mahdi Amin Eltom, research assistant

The role of astrocytes in development and progression of Alzheimer’s disease and Parkinson’s disease

Knowledge about the cellular mechanisms behind the initiation and spreading of Alzheimer’s disease and Parkinson’s disease is still very limited. Decades of research have focused on neuronal abnormalities during the disease progression, but recently more attention has been given to glial cells, including astrocytes. The traditional view of astrocytes solely as structural cells with the main function to hold neurons together has been thoroughly reconsidered. It is now clear that astrocytes are complex cells, playing a number of active roles in both the healthy and the pathological brain. Results from our research show that astrocytes effectively phagocytose (i.e. take up) large amounts of aggregated amyloid-beta and alpha-synuclein. The astrocytes are however extremely slow when it comes to degrading the engulfed material, which is instead stored in the astrocytes for a very long time (Figure 1). Interestingly, we have found that the accumulation of amyloid beta in astrocytes result in secretion of microvesicles, containing partly degraded, extra toxic amyloid beta that induces neuronal cell death.


Being the most numerous glial cell type in the central nervous system, astrocytes have great impact on the brain environment and may constitute a very potent treatment target. The aim with our research is to clarify the involvement of astrocytes in the initiation and progression of Alzheimer’s disease and Parkinson’s disease and to investigate their therapeutic potential.


In our studies we primarily use astrocyte cultures or co-cultures of primary neurons and glia, but we also perform complementary analysis of patient material. To follow different cellular processes we use immunocytochemistry, Western blot analysis and ELISA, as well as time-lapse-, confocal- och electron-microscopy.

Figure 1. Immunostaining of astrocytes
Figure 1. Immunostaining demonstrating that astrocytes (green) accumulate large amounts of amyloid-beta (red) compared to neurons (purple). Cell nuclei are shown in blue.

Selected publications

Rostami J, Fotaki G, Sirois J, Mzezewa R, Bergstrom J, Essand M, Healy L and Erlandsson A (2020). Astrocytes have the capacity to act as antigen-presenting cells in the Parkinson's disease brain. J Neuroinflammation. 17: 119.

Zysk M, Clausen F, Aguilar X, Sehlin D, Syvanen S and Erlandsson A (2019). Long-Term Effects of Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease. J Alzheimers Dis. 72: 161-180.

Sollvander S, Nikitidou E, Gallasch L, Zysk M, Soderberg L, Sehlin D, Lannfelt L and Erlandsson A (2018). The Abeta protofibril selective antibody mAb158 prevents accumulation of Abeta in astrocytes and rescues neurons from Abeta-induced cell death. J Neuroinflammation. 15: 98.

Rostami J, Holmqvist S, Lindstrom V, Sigvardson J, Westermark GT, Ingelsson M, Bergstrom J, Roybon L and Erlandsson A (2017). Human Astrocytes Transfer Aggregated Alpha-Synuclein via Tunneling Nanotubes. J Neurosci. 37: 11835-11853.

Nikitidou E, Khoonsari PE, Shevchenko G, Ingelsson M, Kultima K and Erlandsson A (2017). Increased Release of Apolipoprotein E in Extracellular Vesicles Following Amyloid-beta Protofibril Exposure of Neuroglial Co-Cultures. J Alzheimers Dis. 60: 305-321.

Sollvander S, Nikitidou E, Brolin R, Soderberg L, Sehlin D, Lannfelt L and Erlandsson A (2016). Accumulation of amyloid-beta by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons. Mol Neurodegener. 11: 38.

Loov C, Mitchell CH, Simonsson M and Erlandsson A (2015). Slow degradation in phagocytic astrocytes can be enhanced by lysosomal acidification. Glia. 63: 1997-2009.

Loov C, Hillered L, Ebendal T and Erlandsson A (2012). Engulfing astrocytes protect neurons from contact-induced apoptosis following injury. PLoS One. 7: e33090.

Last modified: 2023-08-22