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Brain geometry matters in Alzheimer’s disease progression: a simulation study

View ORCID ProfileMasoud Hoore, Jeffrey Kelling, Mahsa Sayadmanesh, Tanmay Mitra, Marta Schips, Michael Meyer-Hermann
doi: https://doi.org/10.1101/2020.07.24.220228
Masoud Hoore
1Department of Systems Immunology and Braunschweig Integrated Centre of Systems Biology (BRICS), Helmholtz Centre for Infection Research, Braunschweig, Germany
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  • ORCID record for Masoud Hoore
Jeffrey Kelling
2Department of Information Services and Computing, Helmholtz-Zentrum Dresden - Rossendorf, Dresden, Germany
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Mahsa Sayadmanesh
3Department of Mechanical Engineering, RWTH Aachen University, Aachen, Germany
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Tanmay Mitra
1Department of Systems Immunology and Braunschweig Integrated Centre of Systems Biology (BRICS), Helmholtz Centre for Infection Research, Braunschweig, Germany
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Marta Schips
1Department of Systems Immunology and Braunschweig Integrated Centre of Systems Biology (BRICS), Helmholtz Centre for Infection Research, Braunschweig, Germany
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Michael Meyer-Hermann
1Department of Systems Immunology and Braunschweig Integrated Centre of Systems Biology (BRICS), Helmholtz Centre for Infection Research, Braunschweig, Germany
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  • For correspondence: mmh@theoretical-biology.de
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Abstract

The Amyloid cascade hypothesis (ACH) for Alzheimer’s disease (AD) is modeled over the whole brain tissue with a set of partial differential equations. Our results show that the amyloid plaque formation is critically dependent on the secretion rate of amyloid β (Aβ), which is proportional to the product of neural density and neural activity. Neural atrophy is similarly related to the secretion rate of Aβ. Due to a heterogeneous distribution of neural density and brain activity throughout the brain, amyloid plaque formation and neural death occurs heterogeneously in the brain. The geometry of the brain and microglia migration in the parenchyma bring more complexity into the system and result in a diverse amyloidosis and dementia pattern of different brain regions. Although the pattern of amyloidosis in the brain cortex from in-silico results is similar to experimental autopsy findings, they mismatch at the central regions of the brain, suggesting that ACH is not able to explain the whole course of AD without considering other factors, such as tau-protein aggregation or neuroinflammation.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-ND 4.0 International license.
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Posted July 25, 2020.
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Brain geometry matters in Alzheimer’s disease progression: a simulation study
Masoud Hoore, Jeffrey Kelling, Mahsa Sayadmanesh, Tanmay Mitra, Marta Schips, Michael Meyer-Hermann
bioRxiv 2020.07.24.220228; doi: https://doi.org/10.1101/2020.07.24.220228
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Brain geometry matters in Alzheimer’s disease progression: a simulation study
Masoud Hoore, Jeffrey Kelling, Mahsa Sayadmanesh, Tanmay Mitra, Marta Schips, Michael Meyer-Hermann
bioRxiv 2020.07.24.220228; doi: https://doi.org/10.1101/2020.07.24.220228

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